title: Real time PCR analysis of MSCs co-cultured with sepsis whole blood.

status: Public on Aug 31 2025

city: OTTAWA

first: Shirley

middle: H

last: Mei

state: ON

address: 501 Smythe Road

country: Canada

institute: Ottawa Hospital Research Institute

summary: Mesenchymal stem/stromal cells (MSCs) are actively being explored as a potential therapy for disorders with immune dysregulation, including sepsis. However, little is known about the crosstalk and specific molecular mechanisms underlying the acute inflammatory environment and MSC-mediated immunomodulation of myeloid cells. We utilized ex vivo human and in vivo animal models to perform deep immune phenotyping, investigating the effects of MSCs on neutrophil and monocyte populations during acute inflammation. This was complemented by temporal analysis of neutrophil markers in septic shock patients who received ascending doses of MSC therapy. Our results demonstrated that MSCs positively altered the myeloid cell, promoting anti-inflammatory phenotypes and correcting dysfunctions of myeloid cells. Using MSCs retrieved after exposure to sepsis patient whole blood, transcriptomic and cytokine analyses revealed activation of caspase-1/interleukin-1 converting enzyme pathway as an essential molecular switch mediating immunomodulatory effects of MSCs on dysfunctional neutrophils and monocytes. Notably, non-apoptotic, viable MSCs with caspase-1 activation enhanced the outcome of MSCs to facilitate myeloid modulation, bacterial clearance ex vivo and increase sepsis mice survival in vivo. In contrast, caspase-1 knockdown abolished the ability of MSCs to modulate myeloid cells. Overall, our findings demonstrate an adaptive crosstalk between MSCs and the host immune environment in sepsis-like acute inflammation enhances the therapeutic activity of MSCs. Specifically, MSCs can facilitate pleiotropic modulation of multiple immune cell populations, accelerating immune resolution in sepsis. These novel insights can be leveraged to refine MSC-based therapies.

overall_design: RT-PCR. Qiagen  Profiler PCR Array

first: Yuan

last: Tan


title: Gene expression profile of CPT2-knockdown HCT116 colorectal cancer cells

city: Shenyang

first: Juan

last: Li

address: No.44 Xiaoheyan Road

country: China

institute: Liaoning Cancer Hospital & Institute

type: Expression profiling by high throughput sequencing

summary: CPT2 knockdown induced accumulation of glycerophospholipids and promoted CRC progression. We conducted transcriptomic sequencing of CPT2-knockdown HCT116 CRC cells to explore the underlying mechanism.

overall_design: HCT116 cells in the logarithmic growth phase were treated with either negative control siRNA (NC) or siCPT2 for 48 hours. The cells were collected, washed three times with PBS, and lysed with 1 mL of TRIzol for 5 minutes on ice. The samples were preserved on dry ice and sent to Biomarker Technologies for high-throughput sequencing.

first: Kuo


title: Transcriptome profiling of normal and CYP2E1 knockdown human neural progenitor cells

first: LIN

last: QIN

address: PuHe Road 77

institute: China Medical University

summary: The objective of the study was to examine changes in gene expression induced by CYP2E1 knockdown in neural progenitor cells.There were 6samples in total.Samples shs_1, shs_2, and shs_3 are the control group, and shCYP2E1_1, shCYP2E1_2, and shCYP2E1_3 are the CYP2E1 knockdown group.Neural progenitor cells were cultured in vitro from normal fetal brain tissue aborted at 21 weeks, infected with CYP2E1_shRNAs and CYP2E1_shRNA lentivirus respectively, and then differentiated and cultured for 4 days.The total RNA of each sample was extracted from the lentivirus infected, early differentiated human neural progenitor cells with TRIzol reagent.Then the RNA samples were processed for high throughput transcriptome sequencing on Illumina HiSeq 3000 platform.

overall_design: we employed lentivirus-packaged shRNA to knock down CYP2E1 in primary human neural progenitor cells, which were then cultured for four days before harvest for RNA sequencing.


title: The novel tRF-23 promotes osteogenic differentiation of hBMSCs and protects against bone loss in ovariectomized mice

city: Jiujiang

first: Tao

last: Wang

address: No. 551, Qianjin East Road

institute: Jiujiang University

type: Non-coding RNA profiling by high throughput sequencing

summary: The pathogenesis of osteoporosis is closely related to the impaired human bone marrow-derived stromal cells (hBMSCs) osteogenic differentiation. No studies to date, however, have established whether tRNA-derived fragments (tRFs) can influence osteogenic differentiation of hBMSCs or the onset of osteoporosis. Here, tRF-23 was found to control hBMSC osteogenesis through its ability to target suppressor of cytokine signaling 1 (SOCS1) via the Janus kinase 2/signal transducer and activator of transcription 3(JAK2/STAT3) signaling pathway. tRF-23 was then further established as a potential target for efforts to protect against bone loss and marrow adipose tissue (MAT) accumulation in osteoporotic model mice, and its molecular mechanism was also verified in vivo. Together, these results suggest a model in which tRF-23 can protect against bone loss induced by ovariectomized (OVX) through the augmentation of hBMSC osteogenesis, providing a foundation for further characterizing the pathogenesis of osteoporosis and seeking new therapeutic targets for this disruptive condition.

overall_design: After using Trim Galore to remove any low-quality reads and adapter sequences, the remaining sequences 12-50 nucleotides long were aligned with miRBase (http://www.mirbase.org/). Known miRNAs were identified with BWA followed by the alignment of unmapped reads to rRNAs (https://rnacentral.org/). An in-house tRNA sequence database (using sequences from http://gtrnadb.ucsc.edu/ and https://cm.jefferson.edu/MINTbase/) was then employed for analyses of all other reads that were unmapped. Intronic sequences were initially removed, followed by the addition of CCA to the end of all tRNA sequences. Ultimately, 50 genomic nucleotides were added behind these CCA residues, and the resulting sequences were selected as possible tRFs, followed by classification with tRFdb (http://genome.bioch.virginia.edu/trfdb/) and MINTBase (https://cm.jefferson.edu/MINTbase/). Differentially expressed tRFs during osteogenesis (at days 0, 7, 14 and 21 of osteogenic differentiation) were identified with the EB-Seq algorithm based on the following criteria: fold change > 2 or < 0.5 and P < 0.05, FDR < 0.05. The miRanda and RNAhybrid tools were used to identify predicted targets of these tRFs of interest.

first: Haichun

last: Liao

first: Wen

first: Lin

last: Xu

first: Chao

last: Zhao

first: Xingnuan

first: Jianjun

last: Xiong


title: BehaveSeq: behavioral age-detection in single individuals for reconstruction of high-resolution transcriptional dynamics during development

city: Haifa

first: Nabeel

middle: S.

last: Ganem

address: Stern lab, Faculty of Biology, Technion City, Haifa 3200003, Israel.

department: Biology

country: Israel

institute: Technion - Israel Institute of Technology

summary: Capturing rapid changes in gene expression states across development time is crucial for revealing underlying molecular pathways that organize dynamic developmental processes. Here, we present ‘BehaveSeq’, a framework that integrates behavioral age detection with transcriptomic profiling in the same individuals, to reconstruct minute-resolution developmental profiles of gene expression. By densely sampling isolated C. elegans individuals every ~3 minutes during the L4 stage, we identified thousands of genes showing fast and temporally-structured expression patterns during development. These genes were organized into distinct clusters associated with specific developmental and cellular functions. Further applying the new framework to serotonin-deficient individuals revealed both conserved and altered expression patterns across conditions. Interestingly, using the same single-animal dataset, we were able to train a neural network model to accurately predict the developmental age of each individual solely based on its individual-specific transcriptional signature. Overall, our approach offers a new, generalizable framework for revealing dynamic processes of gene regulation with high temporal precision across the developmental trajectory.

overall_design: Single individual C. elegans RNA seq using SMARTseq2  in multipul time points

middle: S

first: David

last: Scher-Arazi

first: Sharon

last: Inberg

first: Amit

last: Zeisel

first: Shay

last: Stern


title: Elucidating mechanisms of perfluorobutanoic acid (PFBA) exposure in larval zebrafish (Danio rerio).

city: Gainesville

first: Christopher

last: Martyniuk

state: FL

address: 8891 SW 79th Avenue

country: USA

institute: University of Florida

summary: Perfluorobutanoic acid (PFBA) is a short-chain polyfluoroalkyl substance (PFAS) that is measurable in fish tissues and environmental matrices. Previous studies suggest that there are adverse effects on animal and human health following exposure to PFBA, however the mechanisms underlying the toxicity are not well characterized. This study measured biological responses (developmental, transcriptome, and behavioral responses) of zebrafish (wild-type AB strain, Danio rerio) following exposure to a range of PFBA concentrations (0.1-100 µl/L). To further elucidate putative mechanisms related to locomotor abnormalities by PFBA, RNA-seq was conducted.  These data shed new mechanistic light onto the sublethal effects of lesser studied short chain perfluorinated chemicals.

overall_design: For RNA-seq experiments, Samples were collected following the 7-day exposure, transferred to a labeled and pre-weighed 1.7 mL tube. The tube was then immediately flash frozen in liquid nitrogen prior to RNA-seq analysis. A total of 16 RNA samples were used for RNA-seq library construction (RINs>7) (Agilent 2100 Bioanalyzer, Agilent Technologies, Inc.). Exposure groups included 4 treatments:  DMSO control (n=4), 0.1 ug/L PFBA  (n=3), 1 ug/L PFBA  (n=4) and 10 ug/L PFBA (n=5).

first: Chris

first: Amany

last: Sultan

first: Cole

last: English

first: Emma

last: Ivantsova

first: Eliana

last: Maira Agostini Valle


title: DNase I alleviates renal inflammatory injury in MRL/lpr mice by inhibiting NETs formation

city: Hohhot

first: yong

last: jin

address: 1 North Passage Road, Hohhot, Inner Mongolia, China

institute: Inner Mongolia Medical University

summary: Neutrophil extracellular traps (NETs) formation has been closely associated with renal inflammatory injury. We administered DNase I to MRL/lpr mice, monitored signs and renal pathology, quantified gene expression levels, and conducted flow cytometry and RNA-seq analysis. Following DNase I treatment, the lupus-related manifestations, renal pathology, and renal function were significantly improved in the LN mouse model. The expression levels of MPO and CitH3 were reduced, and the expression of inflammatory damage molecules, including IL-1β, TNF-α, and Kim1, was down-regulated. RNA-seq analysis revealed that the neutrophil and T cell activation and chemotaxis pathways were suppressed, and the infiltration of cytotoxic immune cells in the kidneys was decreased in the DNase I-treated group compared to MRL/lpr mice. In conclusion, DNase I alleviates renal inflammatory injury by inhibiting the NETs/TLR4/MYD88 cell signaling axis, reducing the formation of NETs and the infiltration of immune inflammatory cells such as T cells and macrophages. These findings may provide a novel clinical prevention and treatment strategy for LN.

overall_design: To further investigate the potential molecular mechanisms underlying DNase I-targeted NETs in the treatment of LN in a mouse model, we conducted RNA sequencing on kidney tissues from four 21-week-old MRL/lpr mice (Lpr), four MRL/lpr mice treated with DNase I (DNase), and three sex- and age-matched healthy control mice (Ctr).

first: Manling

last: Zhang

first: Xinran

last: Xie

first: Gula

last: Da

first: Hongbin

last: Li

first: Yong

last: Jin


title: New insight into Ginseng root polysaccharide GRP-E1F2 on prodynorphin inhibition to delay senescence-associated neuroaging via modulating cellular senescence

city: changchun

first: Shuai

state: jilin

address: No. 1035 Boshuo Road

department: Northeast Asian Institute of Traditional Chinese Medicine

institute: Changchun University of Chinese Medicine

summary: Neuroaging is one of the most distinct signs of aging, which promotes mild cognitive impairment (MCI) and various neurodegenerative diseases. Previous studies have indicated that Panax ginseng C. A. Mey. (ginseng) root polysaccharides have positive effects against senescence and nerve damage. However, its structure and role in delaying senescence-associated neuroaging have not been comprehensively studied. Therefore, this research characterized the structural features of a ginseng root polysaccharide (GRP-E1F2) and the potential mechanism underlying its anti-neurodegeneration effect against senescence-related function and pathological damage. GRP-E1F2 is a neutral polysaccharide with 11.688 kDa molecular weight, which was isolated from the ginseng roots. In this study, NMR, HPLC, FT-IR, and methylation analyses were performed to identify the physiochemical characteristics of GRP-E1F2, which provided its repetitive unit structures. The in vivo experiments revealed that GRP-E1F2 prolonged the lifespan and mitigated senescence-related symptoms including aggregation of lipofuscin and ROS, as well as the antioxidant enzyme inactivation in aging animals (C. elegans and mice). Furthermore, tert-butyl hydroperoxide (tBHP) induced senescent cells indicated that GRP-E1F2 treated has beneficial anti-aging effects. Moreover, the transgenic C. elegans expressing GFP in D-type gamma-aminobutyric acid (GABA)-positive neurons and mice indicated that GRP-E1F2 reduced neuronal morphological abnormalities and reversed aging-induced cognitive deficits, indicating the anti-neuroaging effects of GRP-E1F2. Mechanistically, GRP-E1F2 downregulates cellular senescence in aging brains and cell models, which was indicated by senescence-associated β-galactosidase (SA-β-gal) activity, marker protein p53, p21, phospho-histone H2A.X, and senescence-associated secretory phenotype (SASP). In addition, RNA-seq, RT-qPCR, and immunofluorescence assays revealed that GRP-E1F2 down-regulated mRNA and protein levels of prodynorphin (Pdyn) in aging models. Moreover, the p53 activator and overexpression vectors of Pdyn were employed to determine the pharmacological mechanism of GRP-E1F2 in reducing Pdyn expressions to delay neuroaging by inhibiting the cellular senescence signaling pathway. This research provides theoretical support and experimental evidence for the clinical application of ginseng root polysaccharides against senescence-associated neuroaging, promoting the modern development of traditional medicines from natural polysaccharides.

overall_design: Male KM mice (5- and 18-month-old) were acquired from the Animal Core Facility of Changchun Yisi Experimental Animal Technology Co. Ltd (Changchun, China). For negative and positive control, 5- and 18-month-old mice received oral physiological saline for 4 weeks every 2 days, respectively. The experiment group comprised 18-month-old mice, who were given 200 mg/kg GRP-E1F2 by gavage for 4 weeks every 2 days

first: Liwei

last: Sun

first: Fangbing

last: Liu

first: Dandan

last: Wang


title: Lack of tolerogenic CD11c+ cells drives early atherosclerosis [scRNA-seq]

city: Lübeck

first: Kristian

last: Händler

address: Ratzeburger Allee 160

department: Human Genetics

country: Germany

institute: UKSH

summary: Atherosclerosis is a chronic disease characterized by both dysregulated lipid metabolism and a sustained inflammatory reaction. To study exuberant inflammation as the main trigger of atherosclerosis, we established a novel in vivo approach to induce predominantly “immune-triggered atherosclerosis” for early atherogenesis independent of lipid dysregulation. Bone marrow from CD11c.DTR-GFP mice, which express the receptor for diphtheria toxin (DT) under control of the CD11c promoter, was transplanted into female C57BL/6 mice, and long-term depletion of antigen-presenting CD11c+ cells following DT administration was achieved without affecting lipid homeostasis. These mice exhibited enhanced atherosclerosis (~300%) in comparison to mice without CD11c+ cell depletion. Interestingly, we observed an altered immune cell composition within the aortic wall, including a decrease in tolerogenic DCs, a shift towards inflammatory Ly6G+/Ly6C+ monocytes and increased CD25+/FoxP3+ T cells, whereby the intracellular cytokine profile showed an increase of TNF- α, INF-γ and IL-17. We furthermore detected a pronounced systemic inflammatory response with increased levels of TNF-α, INFγ, IL-17 and IL-1β. Thus, CD11c+ cells are the decisive cellular brake preventing an exuberant inflammatory response in early atherogenesis. Here, we describe a novel tool for studying the role of immune cells and associated mechanisms in atherosclerosis in mice with intact lipid metabolism.

overall_design: single-nuclei RNA sequencing of aorta samples from C57BL/6 mice fed a standard diet or high cholesterol (HC) diet for 6 weeks using Next GEM Single Cell 3ʹ Kit v3.1 (10X Genomics). 1 replicate each of 3 pooled aorta

first: M

last: Sauter

first: N

last: Anto Michel

first: K

last: Haendler

last: Olbrich

first: H

middle: M

last: Nording

last: Emami

first: G

last: Yücel

first: I

last: Akin

first: A

last: Stanger

first: C

last: Gleissner

last: Schulz

first: S

last: Autenrieth

first: RJ

last: Lengerke

first: D

last: Wolf

last: Duerschmied

last: Stellos

first: T

last: Chavakis

last: Nahrendorf

last: Spielmann

middle: F

last: Langer


title: B-Cells Derived EVs Shape Melanoma Response to Immune Checkpoint Therapy

city: Zurich

first: Richard

last: Chahwan

address: Winterthurerstrasse 190

department: Institute of Experimental Immunology

country: Switzerland

institute: University of Zurich

summary: In recent years, the understanding of the immune tumor microenvironment has evolved to include B cells as active participants rather than mere bystanders. Retrospective studies investigating the presence of B cells and B cells-associated signatures within tumors have revealed a significant correlation with therapeutic outcomes. Although conflicting data exist regarding whether B cells act as pro-tumor or anti-tumor agents, it is becoming increasingly clear that understanding B cells as a heterogeneous population, shaped by tumor microenvironment cues, is essential. This study explores the crucial roles played by B cells and their extracellular vesicles (EVs) in shaping responses to immune checkpoint blockade (ICB) therapy. We have independently verified the significant enrichment of B cells in ICB therapy responders in comparison to non-responder in tumors of melanoma patients. B cell depletion experiments in an in vitro tumor-killing assay demonstrate a clear impairment of T cell-mediated anti-tumor activity. To investigate the clinical relevance, EVs were isolated from melanoma patient tumors, and fractioned into subpopulations, including B cell-derived EVs. MiRNA profiling of CD19+ EVs identifies miR-99a-5p as a top candidate, significantly upregulated in responder EVs. In downstream assays, we observed a B cell-dependent phenotype of miR-99a-5p, where its silencing impaired T cell-mediated anti-tumor cytotoxicity in an in vitro tumor-killing assay. Mechanistically, miR-99a-5p appears to regulate B cell cell-cycle, favoring non-homologous end joining DNA repair pathway, and promoting class-switch recombination. Collectively, data reported herein emphasizes the indispensable role of B cells and their derived EVs in shaping cancer immunotherapy outcome.

overall_design: To investigte the role of B cell-derived EVs in melanoma immunotherapy response

first: Ala'a

last: Hrout


title: Lysine-specific demethylase 6B promotes STAT1-mediated macrophages activation during atherosclerosis development [MeRIP-Seq]

city: hangzhou

first: huan

last: chen

state: Zhejiang

address: Hangzhou, Zhejiang Province, China

institute: Zhejiang Chinese Medical University

summary: Atherosclerosis (AS) induced coronary heart disease is still the first killer threatening human health due to high morbidity and mortality. How N6-methyladenosine modification (m6A) in macrophage participates in atherosclerosis progression is still completely unclear. In this study, by performing meRIP-seq in macrophages during differentiation and activation processes, we aim to understand the landscape of m6A spectrum in macrophage from different stages. Moreover, we also find a large class of histone methylation modification enzymes were regulated by m6A modification. Western blot, qPCR and ChIP-seq results demonstrate m6A modification regulates Lysine-specific demethylase 6B (Kdm6b)-dependent macrophage activation. In mechanism, Kdm6b interacts and methylates Jak1 inducing its phosphorylation-mediated macrophage activation. Furthermore, RIP-qPCR detection indicates following macrophage differentiation and activation, both m6A writers Mettl3 and Rbm15 participates in m6A modification of Kdm6b mRNA. Finally, by performing atherosclerotic model on macrophage-specific Kdm6b knockout mice on Ldlr-/- background, we demonstrate Kdm6b promotes macrophage activation-mediated atherosclerosis by amplifying inflammation and destabilizing plaque. This study will provide a new understanding of the pathogenesis of AS and is expected to develop a new target for the treatment of AS.

overall_design: m6A sequencing data analysis: Effects of IFNγ on m6A modification sites on RNA molecules in mouse bone marrow-derived macrophages


title: Anti-Müllerian Hormone Reduces Uterine DNA Damage and Pregnancy Complications in Doxorubicin-Treated Mice [RNA-seq]

city: Boston

first: Ngoc Minh Phuong

last: Nguyen

state: MA

address: 55 Fruit st

department: Pediatric Surgical Research Laboratory

institute: Massachusetts General Hospital andHarvard Medical School

summary: Anti-Müllerian hormone (AMH) has emerged as a potential fertoprotective agent, demonstrating its strongest protective effects against Doxorubicin (DOX)-induced ovarian toxicity. While chemotherapy’s gonadotoxic impact on ovaries has been extensively studied, its effects on the uterus remain poorly understood. In this study, we investigated DOX-induced uterine damage and assessed the protective role of AMH co-treatment. DOX triggered DNA double-strand breaks in the uterine myometrium, activating Cdkn1a and other Tp53 pathway genes, and was linked to increased dystocia in pregnant mice. AMH co-treatment counteracted these effects by reducing γ-H2AX-positive DNA damage foci, suppressing Tp53 pathway activation, and improving pregnancy outcomes. These findings establish AMH as a promising therapeutic agent for preserving uterine integrity during chemotherapy, opening new avenues for fertility preservation and improved reproductive health in cancer patients.

overall_design: To elucidate the impact of DOX and AMH on prepubertal uterine function, we administered two weekly doses of DOX (3mg/kg) to prepubertal mice (postnatal day 25). A comparative group received concurrent administration of AMH. Uteri were harvested at 4 and 24 hours post-treatment for bulk RNA sequencing analysis.

first: David

last: Pepin


title: Kindlin-2 Orchestrates brown adipose tissue maintenance and thermogenic programing

city: Shanghai

first: Hui

last: Wang

address: Songhu road

institute: Fudan University

summary: Analyze the internal gene changes in brown adipocytes after knockout of Kindlin-2

overall_design: Brown adipocytes were specifically knocked out of Kindlin-2, and the mice were divided into a control group and a knockout group. They were stimulated in a four-degree environment for 6 hours, and the effect of brown adipocyte knockout of kindlin-2 on cold tolerance was observed through cold stimulation.

first: Huanqing

last: Gao


title: Transcriptomics analysis of creeping fat from repeated colonic cautery injury mouse model and healthy controls

city: 济南市

first: xiaofen

last: lv

address: 107 Wenhua West Road

institute: Shandong University

summary: A feature of Crohn's disease is the extra-intestinal manifestation of creeping fat, defined as expansion of mesenteric adipose tissue around the inflamed and fibrotic ileum. We modelled the phenotype by performing repeated colonic cautery in mice. In comparison to healthy controls, we found that the greatest transcriptional changes in creeping fat in mouse model are functions related to collagen production and extracellular matrix organization.

overall_design: We compared the transcriptional activity of creeping fat from repeated cautery mice model and healthy mesenteric adipose tissues from controls.

first: Xiaofen

last: Lv

first: Yunqing

last: Zeng

first: Wenlong

last: Ma


title: RNA-seq of mouse liver from PTENα-/- and WT after LPS treatment

city: Beijing

first: Weixuan

address: No. 38 Xueyuan Road, Haidian District

institute: Peking University

summary: RNA-seq was performed on liver tissues from PTENα knockout and wild-type mice following LPS stimulation. The study aims to characterize gene expression changes associated with hepatic inflammatory responses in the absence of PTENα.

overall_design: We performed gene expression profiling analysis using RNA-seq of liver tissues from PTENα knockout (PTENα-/-) and wild-type (WT) mice. Mice were treated with lipopolysaccharide (LPS, 15 mg/kg, intraperitoneal injection), and liver samples were collected 6 h after stimulation. Total RNA was extracted and subjected to high-throughput sequencing.

first: Linjiang

last: Han

first: Dan


title: Cannabidiol-Induced Recovery of Social Behaviour in Mouse Models of Syndromic Autism

city: Ottawa

first: Vern

last: Lewis

state: Ontario

address: 1125 Colonel By Drive

department: Neuroscience

institute: Carleton University

summary: Despite the growing prevalence of autism, no pharmacological interventions have been approved for core symptoms. The endocannabinoid system (ECS) has recently gained interest as a potential target for treating autism. Cannabidiol (CBD), a compound found in the Cannabis plant (C. Sativa), is a potential autism treatment due to its tolerability and promising early results in fragile X syndrome patients. Here, we aimed to evaluate the efficacy of CBD in treating social deficits and restrictive/repetitive behaviours in two monogenetic models of autism, Shank3 and Fmr1 knock-out (KO) mice. Male and female mice were tested in the 3-chamber social apparatus or for self-grooming and open field test (baseline or pre-treatment), followed by 5 daily treatments of vehicle or CBD (s.c., 5mg/kg for males, 50mg/kg for females) and tested again after the last injection (post-treatment). At baseline and following vehicle treatment, male and female Shank3 and Fmr1 KO mice exhibited deficits in social novelty, which were restored to control levels following CBD administration. Meanwhile, self-grooming (increased in male and female Shank3 KO mice) and open-field exploration (decreased locomotion in Shank3 KO mice) were not affected by CBD. Females had hippocampal CBD levels ~11.6 times higher than males (concordant with the dosing) and presented elevated levels of anandamide (AEA) in the CBD-treated groups. Transcriptomic analysis of the hippocampus revealed a lack of overlap in the CBD differentially expressed genes (DEGs) among the different strains and between sexes. These results suggest sex- and strain-specific mechanisms for CBD and support its therapeutic effects for syndromic autism.

overall_design: RNA-Seq profiling of hippocampal tissue collected from male and female wildtype, Shank3 knockout, and Fmr1 KO mice treated with vehicle or CBD

first: Mike

last: Parkhill

first: Samantha

last: Baglot

first: Brandon

last: Rodrigue

first: Matthew

last: Hill

first: Argel

last: Aguilar-Valles


title: Lack of tolerogenic CD11c+ cells drives early atherosclerosis [RNA-seq]

first: Kristian

last: Händler

overall_design: bulk 5' quantification mRNA-Seq of FACS-sorted mouse bone-marrow-derived CD11c positive cells. 4 replicates each of cells incubated for 24h with acLDL (to mimic an atherosclerotic environment) vs control.

first: M

last: Sauter

first: N

last: Anto Michel

first: K

last: Haendler

last: Olbrich

first: H

last: Nording

last: Emami

first: G

last: Yücel

first: I

last: Akin

first: A

last: Stanger

first: C

last: Gleissner

last: Schulz

first: S

last: Autenrieth

first: R

middle: J

last: Lengerke

first: D

last: Wolf

last: Duerschmied

last: Stellos

first: T

last: Chavakis

last: Nahrendorf

last: Spielmann

last: Langer


title: HNF4α contributes to hepatic CAR dysfunction in polymicrobial sepsis

city: Gent

first: Steven

last: Timmermans

address: Technologiepark 71

country: Belgium

institute: VIB-UGent

summary: Constitutive androstane receptor (CAR) is a xenobiotic nuclear receptor mainly expressed in the liver, where it regulates drug metabolism and energy homeostasis. CAR has emerged as a promising therapeutic target for diabetes, fatty liver disease, and alcoholic liver disease, but it has not been investigated in the context of sepsis. Here, we show that sepsis impairs CAR function in the liver, partly due to reduced transcription mediated by HNF4α, the key liver identity transcription factor, and partly due to decreased DNA binding, caused by chromatin remodelling, also mediated by HNF4α. This impairment leads to the downregulation of several genes involved in monocarboxylic acid, fatty acid, and xenobiotic metabolism, contributing to increased sepsis lethality, and is associated with an  elevated hepatic acute phase response. NCT protects against sepsis by enhancing HNF4α binding to the CAR promoter, thereby increasing both CAR transcription and activity.

overall_design: A total of four conditions were used: SHAM+CTRL, SHAM+TCPOBOP, CLP+CTRL and CLP+TCPOBOP, with 4 biological replicates each, for a total of 16 samples. Livers were isolated and processed for transcriptional profiling by RNA-seq

first: Céline

last: Van Dender

first: Claude

last: Libert


title: Transcriptomic analysis of Ywhaz knockout in preimplantation mouse embryos

city: Wuhan

first: Yuehan

last: Li

address: No. 1095, Jiefang Ave.

institute: Huazhong University of Scicence and Technology

summary: This study investigates the role of Ywhaz in early embryo development using a CRISPR-Cas9 knockout mouse model. RNA-seq was performed on pooled blastocysts derived from control and Ywhaz-knockout zygotes. Differential gene expression and pathway enrichment analysis revealed dysregulation of redox and cell proliferation pathways, providing insights into the molecular function of YWHAZ during preimplantation development.

overall_design: Total of 4 RNA-seq samples: 2 control (Control_1, Control_2) and 2 Ywhaz-knockout (si_Ywhaz_1, si_Ywhaz_2). Each sample consists of a pool of 5 blastocysts. Zygotes were injected with CRISPR-Cas9 targeting Ywhaz or control gRNA, cultured to the blastocyst stage, and pooled for RNA extraction and sequencing.

first: Wenjing

last: Xiong


title: TGFBR1 is an on-off switch for exosome-induced neuroprotection and visual function improvement

city: Changsha

first: Yuerong

last: Ren

address: Renmin Road No.139

institute: central south university

summary: To investigate the neuroprotective role of TGFβR1 in retinal ganglion cells (RGCs),  we isolated adult RGCs from TGFβR1flx/flxvglut2-Cre+/- and TGFβR1flx/flxvglut2-Cre-/- mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for adult RGCs from TGFβR1flx/flxvglut2-Cre+/- and TGFβR1flx/flxvglut2-Cre-/- mice. Three samples each group.


title: Multi-omics analysis highlights the link of aging-related cognitive decline with systemic inflammation and alterations of tissue-maintenance [RRBS]

city: Kiel

first: Lena

last: Best

address: Michaelis-Straße 5

department: Institute of Experimental Medicine

institute: Christian-Albrechts-University Kiel

type: Methylation profiling by high throughput sequencing

summary: Aging-related cognitive decline is associated with changes across different tissues and the gut microbiome, including dysfunction of the gut-brain axis. However, only few studies have linked multi-organ alterations to cognitive decline during aging. Here we report a multi-omics analysis integrating metabolomics, transcriptomics, DNA methylation, and metagenomics data from hippocampus, liver, colon, and fecal samples of mice, correlated with cognitive performance in the Barnes Maze spatial learning task across different age groups. We identified 734 molecular features associated with cognitive rank within individual data layers, of which 227 features remain when integrating all data layers with each other. Among the single-layer predictors, several host and microbial features were highlighted, with host-associated markers being predominant. Host features associated with cognitive function mainly belong to innate and adaptive inflammatory activity (inflammaging) and developmental processes. Our findings suggest that cognitive decline in aging is tightly coupled to systemic, age-associated inflammation, potentially initiated by microbiome-driven gastrointestinal inflammatory activity, emphasizing a link between peripheral tissue alterations and brain function.

overall_design: Reduced representation bisulfite sequencing (RRBS) of 83 genomic DNA samples from male mouse (C57BL/6J/Ukj) hippocampus at different ages: 3 (n = 16), 9 (n = 16), 15 (n = 16), 24 (n = 16), and 28 (n = 18) months.

first: Stefano

last: Flor

first: Thomas

last: Dost

first: Madlen

last: Haase

first: Rowena

last: Simon

first: Marie-Luise

last: Ederer

first: Samer

middle: A

last: Kadibalban

first: Jan

last: Taubenheim

first: Maja

last: Olecka

first: Alesia

last: Walker

first: Johannes

last: Zimmermann

first: Georgios

last: Marinos

first: Sören

last: Franzenburg

first: Philippe

last: Schmitt-Kopplin

first: John

last: Baines

first: Konstantin

last: Riege

first: Steve

last: Hoffmann

first: Christiane

last: Frahm

first: Christoph

last: Kaleta


title: Melanocytes in the mouse inner ear and cells mistaken for melanocytes

city: Jinan

first: Jing

last: Cai

state: Shandong

address: 4 Duanxing West Road

department: Shandong Provincial ENT Hospital

summary: Melanocytes are important components of the inner ear’s cellular architecture. However, limited morphological research has hindered a complete understanding of inner ear function. This study characterized the morphology of inner ear melanocytes and cells often misidentified as melanocytes. Immunofluorescence, Smart-seq, transmission/field emission scanning electron microscopy, and immunoelectron microscopy were used. Cells with a “black ball” appearance in the vestibule were identified as macrophages. We examined variation in melanocytes or macrophages with age, strain, and cisplatin injury. Kir4.1 expression and the greater noise resistance observed in pigmented mice suggest potential melanocyte functions. Based on melanin distribution in Pou3f4y/- mice, we hypothesize that melanocytes migrate from the modiolus along Reissner's membrane to the stria vascularis, following a base to apex gradient. These findings provide novel ultrastructural and immunological insights into inner ear function.

overall_design: Smart-RNA-seq profiling of Cells with a “black ball” appearance in the vestibule.

first: Lei

last: Xu

first: Yongdong

last: Song

first: Aizhen

last: Zhang

first: Zheng

last: Li

first: Boqin

first: Haibo

last: Wang


title: Circadian regulation of transcriptome in spinach leaves under varying nitrogen levels (aligned to Sp75 reference genome)

city: Uvalde

first: Vijay

last: Joshi

state: Texas

address: 1619 Garner Field Road

department: Department of Horticultural Sciences

institute: Texas A&M AgriLife Research

summary: The goal of this study was to compare differentially expressed transcripts in spinach leaves under contrasting nitrogen levels throughout the day and night using transcriptome profiling (RNA-seq)

overall_design: Method:  48-day-old spinach leaf samples (cultivar- Space) were collected from 3 independent plants grown under contrasting levels of nitrogen (high: HN, low: LN) during four different times of the day (T1- End of the dark cycle; T2 – Middle of the light cycle; T3 – End of the light cycle; T4 – Middle of the dark cycle) and were flash-frozen in liquid nitrogen. The homogenized samples were used for total RNA extractions. The T1 set of samples from 3 independent plants under high nitrogen were labeled as  (HNT1_1, HNT1_2, HNT1_3) while under low nitrogen as (LNT1_1, LNT1_2, LNT1_3). Similarly, the samples from the remaining 3-time points under both nitrogen levels were labeled. Messenger RNA was purified from total RNA using poly-T oligo-attached magnetic beads. After fragmentation, the first strand of cDNA was synthesized using random hexamer primers, followed by the second strand of cDNA synthesis using dUTP for directional library. Quantified libraries were pooled and sequenced on NovaSeq X Plus Series, according to effective library concentration and data amount.

first: Benedict

last: Analin


title: RNAseq analysis of Neuro-2a cells after infection with HSV-1

city: Hangzhou

first: Xiang

last: Yuhang

address: Yuhang Tang street

summary: We used HSV-1 to infect Neuro-2a cells (MOI=10) for 5h, and set the mock group without infection as a control. Host genes that were significantly changed between HSV-1 infected and control groups were compared.

overall_design: We focused on genes that were significantly up-regulated or down-regulated in the infected group compared to the control group. Three replicates were set for each group, named MOCK1, MOCK2, MOCK3, HSV1, HSV2, and HSV3.

first: Dongli

last: Pan

first: Yuhang

last: Xiang


title: Therapeutic restoration of mitochondria–endoplasmic reticulum crosstalk for osteoarthritis

city: Suzhou

first: Mingzhuang

last: Hou

address: Pinghai Street 899#

institute: Suzhou University

summary: Osteoarthritis is a prevalent joint disease in the aging population. The hallmark of osteoarthritis is the degeneration of the joint cartilage, characterized by changes in chondrocytes including mitochondrial dysfunction. However, the precise mechanisms of how this affects chondrocyte homeostasis and whether such processes can be explored as therapeutic targets for osteoarthritis remain unclear. Here, we show that impaired mitochondrial function and disrupted cartilage matrix metabolism due to loss of mitofusin-2 (MFN2) expression in chondrocytes leads to the development of osteoarthritis. Sirtuin-3 (SIRT3), a key regulator of mitochondrial function, plays a critical role in modulating MFN2 to restore mitochondrial dynamics, reduce fragmentation, and preserve mitochondrial function in chondrocytes. Specifically, SIRT3 directly deacetylates and indirectly deubiquitinates MFN2, preventing its degradation. MFN2-mediated mitochondrial–endoplasmic reticulum (ER) junctions support cellular homeostasis, alleviate ER stress, and maintain mitochondrial calcium ion balance, which collectively mitigate chondrocyte senescence. Extracellular vesicles engineered with MFN2 mRNA effectively prevented cartilage degeneration and restored mobility in osteoarthritic mice. These findings suggest that targeting MFN2 is a promising strategy to prevent cartilage degeneration and alleviate progression of osteoarthritis.

overall_design: We performed gene expression profilling analysis using data obtained from RNA-seq of chondrocytes derived from MFN2wt and MFN2Col2a1-/- mice.

first: Yaoge

last: Deng


title: Elucidating mechanisms of PFDoDA exposure in larval zebrafish (Danio rerio)

city: Gainesville

first: Christopher

last: Martyniuk

address: 8891 SW 79th Avenue

institute: University of Florida

summary: Seven day old larval fish were exposed to one of two concentrations of PFDoDA. RNA-seq was conducted on pools of fish

overall_design: For RNA-seq experiments, Samples were collected following the 7-day exposure, transferred to a labeled and pre-weighed 1.7 mL tube. The tube was then immediately flash frozen in liquid nitrogen prior to RNA-seq analysis. A total of 9 RNA samples were used for RNA-seq library construction (RINs>7) (Agilent 2100 Bioanalyzer, Agilent Technologies, Inc.). Exposure groups included 3 treatments:  DMSO control (n=3), 0.1 ug/L (n=3), and 10 ug/L (n=3).

first: Victoria

last: Lopez-Scarim

first: Cole

last: English

first: Lev

last: Avidan

first: Mario

last: Rivera


title: Effects of Hikeshi Deficiency on Neural Stem Cell Proliferation and Differentiation

city: shanghai

first: Debao

last: Wu

state: Shanghai

address: Chongqing Nanlu 227

institute: Shanghai Jiao Tong University

summary: To investigate the effects of Hikeshi deficiency on neural stem cells, we isolated NSCs from wild‑type and hGFAP‑Cre; Hikeshi f/f mice and performed RNA‑seq analysis.

overall_design: RNA‑seq was conducted on neural stem cells isolated from wild‑type and Hikeshi conditional knockout (cKO) mice.

first: Li

first: Ximing

last: Nian

first: Liang


title: Altered expression of long noncoding RNAs regulating neutrophilic inflammation in peripheral blood was associated with symptom severity in patients with house dust mite-induced allergic rhinitis

first: Jinming

last: Zhao

state: Beijing

address: No.1, Dongjiaominxiang, Dongcheng District

institute: Beijing Tongren Hospital, Capital Medical University

summary: Long noncoding RNAs (lncRNAs) have been implicated in a diverse array of human immune diseases; however, a comprehensive understanding of the expression and function of lncRNAs in the peripheral blood leukocytes of individuals suffering from house dust mite (HDM)-induced allergic rhinitis (AR) remains elusive.

overall_design: To explore the potential roles and functions of long noncoding RNAs (lncRNAs) in the pathogenesis of AR. Sequencing analysis was performed on peripheral blood leukocytes collected from patients with HDM-induced AR and healthy controls (HCs) to elucidate the expression patterns of lncRNAs. Differentially expressed (DE) lncRNAs were identified and validated, and further correlation analyses were conducted to explore their associations with visual analog scale (VAS) scores and cytokine levels in the serum and nasal secretions. Additionally, bioinformatics analyses were performed to predict the potential pathways influenced by DE lncRNAs. Finally, the diagnostic potential of these lncRNAs in AR was assessed via receiver operating characteristic (ROC) curve analysis.

first: Xiaoyu

last: Pu

first: Xiangdong

first: Luo

last: Zhang


title: Transcriptomic adaptations of Clostridium thermocellum strains evolved to grow on xylose

city: Golden

first: Katherine

last: Chou

state: CO

address: 15013 Denver West Parkway

department: Biosciences Center

institute: NREL

summary: A strain of Acetivibrio thermocellus (colloquially, Clostridium thermocellum) DSM 1313 capable of growing in xylose was created by both rational engineering and adaptive laboratory evolution (ALE) approaches. This RNA-seq experiment compares the transcriptomes of the pre-ALE strain on native substrate with the pre-ALE and post-ALE strains growing in xylose (or xylose plus xylan).  These data show the progression of the initially engineered strain from normal growth with a native substrate, to debilitated growth in the new engeered substrate, to improved growth on the engineered substrate after ALE. Genes of various biological functions are found to undergo coordinated changes at various stages of the engineering & ALE campaign. These correlations shed light on the state of the cell at each stage. All together, these data paint a picture of the strain initially undergoing a stress state, which is eventually overcome through ALE. Many of these changes dissipate in the fast growing strain, leaving only permanent changes that enable growth on xylose.

overall_design: Strain KJC355 is A. thermocellus DSM 1313 Δhpt with xylA and xylB genes integrated into the hpt locus. KJC335 was subjected to ALE producing strains KJC19-9 and KJCXn4 which were adaped to growth on xylose or xylose plus xylan, respectively. GSE137509 includes data for KJC355 in cellobiose (native substrate) and xylose (engineered substrate). This submission includes data for KJC19-9 grown in xylose, KJCXn4 grown in xylose + xylan, and KJCXn4 grown in xylose alone.

first: Skyler

middle: D

last: Hebdon

first: Christine

last: Kelly

first: Albert

middle: E

last: Tafur Rangel

first: Luis

last: Reyes

first: Trevor

last: Croft


title: The interaction of CDC6 and Tmod3 accelerates resistance to paclitaxel through focal adhesion assembly

first: Yue

last: Liu

address: No. 44 West Wenhua Road

department: School of Pharmaceutical Science

summary: The widespread clinical application of paclitaxel (PTX) in cancer treatment has been significantly limited by the emergence of drug resistance and drug-tolerant persisters. Through genome-wide CRISPR/Cas9 screening, we identified cell division cycle 6 (CDC6) as a critical determinant of cell adhesion-mediated paclitaxel resistance. CDC6, an essential DNA replication licensing factor, functions through a pathway distinct from well-characterized resistance mechanisms. The depletion of CDC6 considerably increases paclitaxel-induced cell death. Beyond its established role in stabilizing chromosomes, our findings indicate that tropomodulin-3 (Tmod3) interacts with CDC6 in the cytoplasm. This interaction enhances CDC6 protein stability and drives drug-resistant phenotypes through regulating actin cytoskeleton remodeling and facilitating focal adhesion assembly. In addition, pharmacological or genetic inhibition of CDC6 notably sensitizes the antitumor efficacy of paclitaxel both in vitro and in vivo. Collectively, our studies elucidate the mechanisms through which CDC6 functions as a key regulator of paclitaxel resistance and provide a potential strategy to enhance paclitaxel efficacy through cytoskeletal-adhesion axis modulation.

overall_design: RNA sequencing was performed on paclitaxel-sensitive and resistant cell lines to identify differentially expressed genes.

first: Huirui

last: Wang

first: Jie

last: Zhan

first: Jiabo

last: Sun

first: Yan

first: Xiaojie

last: Fu

first: Dongxue

last: Lv


title: RNA sequencing of cultured mouse pancreatic bud

city: Yokohama

first: Airi

last: Inoue

state: Kanagawa

address: 4259 Nagatsuta-cho, Midori-ku

country: Japan

institute: Tokyo institute of technology

summary: Our RNAseq showed that VMAT2 inhibition to pancreatic bud from E12.5 for 2 days promoted pancreatic branching morphogenesis and differentiation. The Genes associated with antioxidant activity was also changed, which indicated the possible involvement of ROS in branching morphogenesis.

overall_design: To gain insights into the molecular mechanism underlying the impact of the VMAT2-monoamine pathway on pancreatic development, we conducted RNAseq to analyze the global expression profiles of Tetrabenazine (TBZ)-treated and control pancreatic buds cultured from E12.5, for 2 days.


title: Cannabidiol Modulates Odonto/Osteogenic Differentiation In Human Dental Pulp Stem Cells

city: Bangkok

first: Ajjima

last: Chansaenroj

address: 34 Henri-Dunant Road

department: Anatomy

country: Thailand

institute: Faculty of Dentistry, Chulalongkorn University

summary: Canabidiol (CBD), derived from Cannabis sativa plant exhibits beneficial in alleviating a number of  of oral and dental pathoses This study aimed to explore the impact of CBD on several traits of human dental pulp stem cell (hDPSC) such as their proliferation, apoptosis, migration, and odonto/osteogenic differentiation. hDPSCs were harvested from human dental pulp tissues. The cells were treated with 1.25, 2.5, 5, 10, 25, and 50 μg/mL CBD. Cell response in terms of cell proliferation, colony-forming unit, cell cycle progression, cell migration, apoptosis, and odonto/osteogenic differentiation of hDPSCs were assessed in normal and P. gingivalis lipopolysaccharide (LPS)-induced `inflammatory` milieus. RNA sequencing and proteomic analysis were performed to predict target pathways impacted by CBD. In a normal physiological growth milieu, exposure to 5 μg/mL CBD attenuated hDPSCs proliferation and reduced the number of colony-forming units. On the contrary, in LPS-exposed hDPSCs, a dose of 1.25 μg/mL CBD restored proliferation and odonto/osteogenic differentiation. Proteomic analysis demonstrated that several proteins involved in cell proliferation and differentiation were upregulated following CBD exposure, including CCL8, CDC42, and KFL5. RNA sequencing data indicated that CBD upregulated Notch signaling pathway. In an inhibitory experiment, DAPT, a Notch inhibitor, reduced the effect of CBD-rescued LPS-attenuated mineralization in hDPSCs, suggesting that CBD potentially mediates Notch activation to exert its effect on odonto/osteogenic differentiation of hDPSCs. CBD recovers the proliferation and survival of hDPSCs following exposure to LPS. Additionally,we report here, for the first time, that CBD-mediated Notch activation effectively restores the odonto/osteogenic differentiation ability of hDPSCs. These results while uncovers and underscore the potential role of CBD as a therapeutic option to enhance dentin regeneration.

overall_design: hDPSCs were harvested from human dental pulp tissues. The cells (n=3) were treated with 1.25 μg/mL CBD compared to the growth medium control. RNA sequencing were performed to predict target pathways impacted by CBD.

first: Chatvadee

last: Kornsuthisopon

first: Ravipha

last: Suwittayarak

first: Suphalak

last: Phothichailert

first: Khunakon

last: Usarprom

first: Apicha

last: Srikacha

first: Sornkanok

last: Vimolmangkang

first: Chaloemrit

last: Phrueksotsai

first: Lakshman

middle: P

last: Samaranayake

first: Thanaphum

last: Osathanon


title: Myeloid-specific deletion of Capns1 attenuates myocardial infarction injury via restoring mitochondrial function and inhibiting inflammasome activation

first: zilong

last: xiao

address: Xietu Road1609, Xuhui District

department: cardiology

institute: fudan university

summary: Mitochondrial dysfunction of macrophage-mediated inflammatory response plays a key pathophysiological process in myocardial infarction (MI). Calpains are a well-known family of calcium-dependent cysteine proteases that regulate a variety of processes, including cell adhesion, proliferation, and migration, as well as mitochondrial function and inflammation. CAPNS1, the common regulatory subunit of calpain-1 and 2, is essential for the stabilization and activity of the catalytic subunit. Emerging studies suggest that calpains may serve as key mediators in mitochondria and NLRP3 inflammasome. This study investigated the role of myeloid cell calpains in MI. MI models were constructed using myeloid-specific Capns1 knockout mice. Cardiac function, cardiac fibrosis, and inflammatory infiltration were investigated. In vitro, bone marrow-derived macrophages (BMDMs) were isolated from mice. Mitochondrial function and NLRP3 activation were assessed in BMDMs under LPS stimulation. ATP5A1 knockdown and Capns1 knock-out mice were subjected to MI to investigate their roles in MI injury.   Ablation of calpain activities by Capns1 deletion improved the cardiac function, reduced infarct size, and alleviated cardiac fibrosis in mice subjected to MI. Mechanistically, Capns1 knockout reduced the cleavage of ATP5A1 and restored the mitochondria function thus inhibiting the inflammasome activation. ATP5A1 knockdown antagonized the protective effect of Capns1 mKO and aggravated MI injury. Conclusion: This study demonstrated that Capns1 depletion in macrophages mitigates MI injury via maintaining mitochondrial homeostasis and inactivating the NLRP3 inflammasome signaling pathway. This study may offer novel insights into MI injury treatment.

overall_design: comparative gene trabscription of RNA-seq data for capns1 KO BMDMs and wt BMDMs

first: Zilong

last: Xiao

first: Xiang

last: Wei

first: Yixiu

last: Liang

first: Ziqing

last: Yu


title: Effect of knockdown of GRIK1 on gene expression dring glioblastoma progression

first: hou

middle: guo

last: qiang

address: 160 pujian road

department: Neurosurgery

institute: Department of Neurosurgery, Renji Hospital, Shanghai Jiaotong University, Shanghai, China

summary: Glioblastoma (GBM) is the most aggressive cancer in brain and contains a high mortality rate due to lack of effective treatment strategy. Molecular mechanisms of GBM characteristic invasive growth are urgently need to improve the poor prognosis.Here we reported that knockdown of GRIK1 retarded GBM cells growth and invasion.Moreover,high levels of GRIK1 were correlated to poor prognosis of GBM, consistent with The Cancer Genome Atlas (TCGA) database. Taken together, our study identified that GRIK1 is a novel and vital factor of GBM progression and may serve as a new biomarker for prognosis and therapy of GBM patients.

overall_design: To investigate the downstream mechanism of GRIK1 in GBM progression, we established U87-MG cells in which GRIK1 was knockdown by shRNA.We then performed gene-expression profile analysis using data obtained from RNA-seq of these cells. Comparative gene expression profiling analysis of RNA-seq data for U87-MG and its KD derivative.

first: Hou

last: Guoqiang

first: Xu

last: Xinhang

first: Hu

last: Weixing

first: Ji

last: Jing


title: PML functions as SUMO E3 for microprocessor and modulates global miRNA biogenesis

city: RTP

first: Xiaojiang

last: Xu

state: North Carolina

address: 111 T. W. Alexander Dr.,

institute: NIEHS

summary: The goal is to test if promyelocytic leukemia protein (PML) enhances miRNA biogenesis at a global level by regulating the microprocessor. Nuclear PML isoforms directly interact with ribonuclease III enzyme Drosha and robustly promote the processing of primary to precursor miRNAs.

overall_design: The experiments include testing changes in miRNAs in 1) PML Knockout cells and 2) AD cortex where PML is downregulated.

first: Mao

last: Zixu

first: Li

last: Wenming


title: Targeting STAT3-FoxO1 axis reverses de novo and acquired PARP inhibitor resistance independent of BRCA status [RNA-seq]

city: Xiamen

first: Qing

last: Li

address: School of Life Sciences, Xiang'an Campus, Xiamen University, Xiang'an District

institute: xiamen university

type: Genome binding/occupancy profiling by high throughput sequencing

summary: PARP inhibition has been approved as a compelling strategy for treating multiple human cancers bearing homologous recombination defects (HRD). However, due to the lack of functional biomarkers of PARPi response beyond known genetic mutations in HRD genes, expanding the potential benefit of PARP inhibitors, as well as the identification of effective therapeutic strategies for treating PARPi-resistant cancers remain urgent unmet needs. Here, we report high levels of FoxO1, either at basal expression or upon induction by PARPi, render both BRCA-proficient (BP) and BRCA-deficient (BD) human cancers resistant to PAPRi via modulating transcriptomic signature regulating DNA damage response (DDR). We further elucidated that PARPi-induced STAT3 activation, which occurred through its attenuated dephosphorylation at Y705, resulted in enhanced FoxO1 transcription via recruiting TOP2A, a downstream target of FoxO1. TOP2A orchestrated STAT3-dependent transcriptional program via facilitating RNA Pol II recruitment to gene promoters, as well as promoter-proximal pausing and pause release. Intriguingly, STAT3 inhibitor exhibits a potent synergistic effect with PARPi in treating BP or BD PAPRi-resistant PDX models across cancer types. Our data highlight a potential role of FoxO1 serving as both predictive and prognostic marker for PARPi treatment, and reveal the potency of combination treatment strategy using STAT3 inhibitor with PARPi in sensitizing PARPi-resistant cancers, regardless of BRCA status.

overall_design: RNA-seq was perform to illustrate potential biomarker for predicting PARPi sensitivity and targets regulated by FoxO1/STAT3/TOP2A.

first: Han

last: You

first: Chen

last: Liu

first: Tong

last: Shu

first: Min

last: Zheng


title: Elevated VAMP8 Expression Promotes Cervical Cancer Progression by Enhancing Autophagy via HIF-1 Pathway

status: Public on Aug 30 2025

first: dan

last: wu

address: shengyang road

institute: Obstetrics and Gynecology Hospital of Fudan University

summary: Background: Cervical cancer, prevalent in low- and middle-income countries, is primarily caused by high-risk HPV16. Vesicle-Associated Membrane Protein 8 (VAMP8), involved in vesicle trafficking and autophagy, may influence HPV16-related cervical cancer progression.  Methods: VAMP8 expression was evaluated in cervical tissue specimens from patients with HPV16-positive lesions (including low- and high-grade squamous intraepithelial lesions and cancer) and HPV-negative normal controls using proteomics, qPCR, and immunohistochemistry. A Cox proportional hazards model for prognosis was developed using immunohistochemical data from a cohort of cervical cancer patients. The clinical significance of VAMP8 was further assessed using RNA-seq and clinical data from The Cancer Genome Atlas-Cervical Cancer (TCGA-CESC) cohort. The effects of VAMP8 on autophagy and tumor progression were examined in HPV16 E6/E7-immortalized cervical epithelial cells (Ect1/E6E7) and cervical cancer cell lines (SiHa, HeLa, C-33A) in vitro, and in a SiHa xenograft model in vivo. Transcriptomic analysis of Ect1/E6E7 and SiHa cells identified VAMP8-regulated pathways. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays in SiHa cells were used to confirm the regulation of the HIF-1 pathway.  Results: VAMP8 was upregulated in HPV16-positive samples, particularly in low-grade squamous intraepithelial lesions (LSIL). Elevated VAMP8 correlated with poor survival outcomes and advanced tumor stages. VAMP8 enhanced autophagy and reduced proliferation and invasiveness in HPV16-positive cervical cells but increased in established cancer cell lines. In vivo, VAMP8 overexpression promoted tumor growth and autophagy. The HIF-1 pathway emerged as a key regulatory axis of VAMP8, enhancing hypoxic responses and angiogenesis.  Conclusion: Elevated VAMP8 in HPV16-associated cervical cancer promotes tumor progression by enhancing autophagy via the HIF-1 pathway, suggesting its potential as a diagnostic and prognostic biomarker.

overall_design: RNA-seq Profiling of Wild-Type ECT-1/E6/7, siHA Cells, and Their VAMP8-Overexpressing  Derivatives (OEVAMP8)

first: Yue

last: Wang

first: Dan

last: Wu

first: Jinxia

last: Gai

first: Yiying

last: Cai

first: Keqin

last: Hua

first: Zhiling

last: Zhu

first: Weijuan

last: Xin


title: TGF-β signaling mediates microglial resilience to age-dependent dorsal column myelin alterations

city: Stockholm

first: Keying

state: -- select state --

address: L8:04, Center for Molecular Medicine, Karolinska University Hospital

country: Sweden

institute: Karolinska Institutet

summary: Microglia survey and regulate central nervous system myelination during development and homeostasis. However, whether microglia-myelin interactions are anatomically regulated remains unexplored. Herein, by exploring the spinal cord, which contains several white matter tracts, we demonstrate age-dependent myelin ultrastructural abnormalities occurring in the dorsal column (DC) but not the ventral column (VC). Transcriptomic analyses comparing aged and young spinal cords reveal major changes in genes regulating myelin, microglial function, and the TGF-β signaling pathway. The TGF-β signaling pathway is upregulated in the spinal cord with aging, and a TGFβ-enriched microenvironment is induced in the DC. Disrupting TGFβ1-TGFBR1/2 axis in microglia, by altering either ligand or receptor expression, leads to increased microglial activation, abnormal phagocytic behavior, and myelin loss in the DC, accompanied by neurological deficits more severe in older mice. snRNA-seq reveals a TGF-β signaling-sensitive microglial subset in the spinal cord, spatially restricted in the DC. These findings demonstrate that TGF-β signaling is indispensable for maintaining microglial resilience to myelin alterations in the DC during the aging process, highlighting a previously unresolved checkpoint mechanism of TGF-β signaling with regional specificity.

overall_design: To understand the transcriptomic changes of microglia in the spinal cord following Tgfbr2 deletion, we sorted 100 microglia from the spinal cords of Cx3cr1CreER:Tgfbr2fl/fl mice from the dorsal column (DC), ventral column (VC), and grey matter (GM) at 18 and 28 days post tamoxifen injection. Tgfbr2fl/fl mice were used as the wildtype control.

first: Robert

last: Harris

first: Harald

last: Lund


title: 4T1 cells treated by Astragalin

city: Chongqing

first: Si-zhen

last: Yang

state: Chongqing

address: Gaotanyan Street, No.30

institute: Army Medical University

summary: 4T1 breast cancer cells were treated by Astragalin, to detect the effects of Astragalin on the cellular fate of 4T1 cells

overall_design: 4T1 cells were treated with AS at 20μM for 24 hrs in vitro

first: Ying

last: Zhang

first: Xu

last: Hu

first: Tong-wei

last: Chu


title: Immune recovery in tumor microenvironment of TP53-mutated AML following venetoclax combination therapy

city: Tokyo

first: Kohei

last: Yamada

address: 2-1-1, Hongo, Bunkyo-ku

institute: Juntendo university

summary: The BCL-2 inhibitor venetoclax combined with the hypomethylating agent azacitidine or with low-dose cytarabine significantly improves response rates and overall survival (OS) for newly diagnosed unfit and relapsed / refractory (R/R) acute myeloid leukemia (AML) patients. We retrospectively analyzed our experience with venetoclax combination therapy in 41 unfit AML patients (23 untreated, 18 R/R). Overall response rates were 78.3% for untreated patients and 61.1% for R/R patients. TP53 alterations were observed in 13 patients (31.7%) and were identified as an independent predictor of poor outcome (p=0.0008). We further conducted single-cell RNA sequencing in bone marrow, sampled before and after venetoclax and azacitidine treatment, of three TP53-mutated AML patients who achieved complete remission (CR) or CR with incomplete hematologic recovery. After treatment, numbers of cells expressing anti-apoptotic genes such as BCL2 and MCL1 decreased. CD4 T cells, cytotoxic CD8 T cells, and NK cells significantly increased both in number and in levels of gene expression associated with cytotoxicity post-treatment, confirming immune recovery in the tumor microenvironment. Residual AML cells expressed CD47 and CLEC12A (CLL1). These results indicate that venetoclax combination therapy of AML is promising in real-world clinical practice and suggest a role for ancillary treatment targeting antigens expressed on residual AML cells as a therapeutic strategy in TP53-mutated AML.

overall_design: To investigate how venetoclax and azacitidine therapy affected tumor microenvironment of TP53-mutated AML, we analyzed gene expression by scRNA-seq in bone marrow samples obtained pre- and post-treatment from 3 untreated patients with TP53-mutated AML (AML-15, 16, 27) (Figure 2C). Post-treatment marrow was sampled 1 month after starting standard-dose venetoclax and azacitidine therapy. The status of AML-15 was assessed as CRi and that of AML-16 and -27 was assessed as CR.

first: Kota

last: Tachibana

first: Miki

last: Ando


title: A new Ribociclib derivative, Rib-GW, exerts anti-breast cancer effects through activation of the endogenous apoptotic pathway

city: 连云港

first: J

last: W

address: 江苏省连云港市海州区苍梧路59号

institute: 江苏海洋大学

summary: RNA sequencing and bioinformatics analysis revealed 1,187 differentially expressed genes, and functional enrichment analysis showed that these genes were significantly associated with the apoptosis pathway.

overall_design: To study the role and mechanism of Rib_GW in breast cancer, we conducted Rib_GW treatment and untreated control experiments on MDA-MB-231 cells. Subsequently, we performed gene expression profiling analysis using RNA sequencing data from the Rib_GW treatment group and the DMSO control group.

first: Jian

first: Jing

last: Ji


title: Lentiviral-mediated phenotypic correction of type 1 and type 2 ABCA3 pathogenic variants

city: Boston

first: Pushpinder

last: Bawa

state: Massachusetts

address: 670 Albany St

department: Boston University Medical Campus

institute: Center for Regenerative Medicine

summary: The ATP-binding cassette subfamily A member 3 (ABCA3) protein localizes to lamellar bodies in alveolar type 2 (AT2) cells and transports phospholipids required for pulmonary surfactant assembly. ABCA3 deficiency results from biallelic pathogenic variants in ABCA3 and causes progressive neonatal respiratory failure or childhood interstitial lung disease (chILD). Supportive care or lung transplantation are the only current treatments for ABCA3 deficiency. Complementing defective ABCA3 production by gene addition has therapeutic potential. Previous studies show that repairing or complementing ABCA3 in induced pluripotent stem cell (iPSC) derived AT2 cells restores defining phenotypes (e.g., lamellar body morphology and surfactant phospholipid composition). ABCA3 pathogenic missense variants are rare or private and disrupt ABCA3 function through altered protein trafficking (type 1) or impairing phospholipid transport (type 2) into the lamellar bodies. Little is known about cellular responses to complementing mistrafficking or phospholipid transport variants. Here we used CRISPR/Cas9 to knockout ABCA3 from the A549 human pulmonary epithelial cell line to generate A549/ABCA3-/- cells stably expressing ABCA3 missense variant cDNAs from a single genomic locus: L101P (type 1), E292V (type 2), or E690K (type 2), or wild-type cDNA. Lentiviral-mediated ABCA3 delivery to each cell line phenotypically corrected the mutant cells. We observed restoration of lamellar body morphology and cell proliferation in ABCA3 complemented cells. Bulk RNA sequencing suggested that ABCA3 delivery ameliorated aberrant NF-kB signaling in p.E292V or p.E690K mutant cell lines, but not in p.L101P or knockout lines. These studies highlight important differences between ABCA3 pathogenic variant types that may influence genetic therapy outcomes.

overall_design: RNA-seq profiling of A549 cell lines including wild-type, ABCA3 knockout, and ABCA3 variants including L101P, E292V, and E690K. Each line was transduced with a gene therapy lentiviral vector expressing ABCA3:GFP.

first: Ashley

middle: L

last: Cooney

first: Darrell

middle: N

last: Kotton

first: Paul

middle: B

last: McCray Jr


title: Treatment of prostate cancer with oncolytic virus OH2 [bulkRNA-seq_tumors]

city: Wuhan

first: Jinzhou

last: Xu

state: Hubei

address: Jiefang Avenue

institute: Tongji Hospital

summary: Prostate cancer is a major challenge due to limited treatment options in advanced stages. Immunotherapy has shown promising prospects in various cancers, but it faces obstacles in prostate cancer due to its immunosuppressive microenvironment and low response rate to current therapies. Oncolytic virus therapy provides a new immunotherapy approach by stimulating anti-tumor immune responses. This study investigated the histological changes of the novel herpes simplex virus type II (HSV-II) oncolytic virus OH2 in prostate cancer tumors.

overall_design: Prostate cancer subcutaneous transplanted tumors (RM-1, 5 vs. 5) were treated with oncolytic virus OH2 intervention

first: Ye

last: An

first: Guichen

last: Ye

first: Zhiyu

last: Xia

first: Shaogang

last: Wang

first: Qidong


title: Genome-wide DNA methylation profiles of liver tissue samples obtained from patients with metabolic dysfunction-associated steatohepatitis (MASH), with or without hepatocellular carcinoma

city: Shinjuku-ku

first: Yae

last: Kanai

state: Tokyo

address: 35 shinanomachi

department: Pathology

institute: Keio University School of Medicine

type: Methylation profiling by genome tiling array

summary: Genome-wide DNA methylation profiling was performed on non-cancerous and cancerous liver tissue samples obtained from patients with MASH using the Illumina Infinium HumanMethylation450 BeadChip.

overall_design: 41 genomic DNA was extracted form FFPE specimens obtained from partial hepatectomy materials of 31 patients, who had provided written informed consent. Genomic DNA was subjected to bisulfite conversion followed by Infinium assay.

first: Junko

last: Kuramoto

first: Kimberley

last: Evason


title: Establishing a Canine Urothelial Carcinoma Organoid Repository: A Platform for Comparative and Translational Studies [RNA-Seq]

city: Ames

first: Christopher

last: Zdyrski

state: Iowa

address: 1800 Christensen Dr, Bms 1072 Vet Med, Bms 1072 Vet Med

institute: Iowa State University

summary: Despite the increasing number of treatment options for patients with muscle-Invasive Bladder Cancer (MIBC), many of these patients ultimately have a poor prognosis. Drug responses vary considerably among patients and in many who respond initially, drug resistance may ultimately develop leading to tumor progression. Scope for improvement has been limited by the phenotypic and molecular diversity of MIBC, which impact the selection pressures of therapy. To address this translational gap, we describe the largest known canine urothelial carcinoma organoid bioarchive, with in-depth phenotypical and molecular characterization. Immunohistochemistry confirmed the expression of key biomarkers including UPKIII, E-cadherin, Vimentin, and Ki-67 in organoids. Single-nucleus RNA sequencing revealed cellular heterogeneity, while bulk RNA sequencing showed canine patient-to-patient variability in transcriptomic profiling. Bulk RNA sequencing also displayed highly similar expression profiles between tissue- and urine-derived organoids, as well as similarity to human MIBC transcriptome data. Whole genome sequencing in a subset of patients further supported the overall genomic fidelity of organoids with their tissue of origin. Finally, for proof-of concept of functional usefulness, organoid cytotoxicity to vinblastine was tested in several organoid lines. These canine bladder cancer organoid lines can be thawed, expanded, and screened for response to potential novel therapeutics to expand personalized medicine approaches. In addition, the organoid lines can serve as a valuable resource for comparative bladder cancer research, and as a pre-clinical screening tool to identify efficacious drugs before taking them into canine clinical trials to support future human clinical trials.

overall_design: RNA-seq profiling of canine bladder cancer tissues and organoids which were either urine or tissue derived.

first: Karin

last: Allenspach

first: Jonathan

last: Mochel


title: Establishing a Canine Urothelial Carcinoma Organoid Repository: A Platform for Comparative and Translational Studies [snRNA-Seq]

overall_design: RNA-seq profiling of a canine bladder cancer patient tissue and organoid line.


title: Stop and smell the grasses: evolution of scent producing genus Cymbopogon

city: Rio de Janeiro

first: Luis

middle: Willian

last: Pacheco Arge

state: Rio de Janeiro

address: Av. Carlos Chagas Filho, 373

department: Genetica

country: Brazil

institute: UFRJ

summary: Cymbopogon spp. are grass species widely used around the world as medicinal plants and in various industries for the production of perfumes and pharmaceuticals. Despite their extensive use, there are relatively few studies at the genomic and transcriptomic levels. In this study, transcriptomic data were generated for two species—Cymbopogon flexuosus and Cymbopogon winterianus—to investigate evolutionary aspects and the expression of genes associated with secondary metabolite biosynthesis. The transcriptome assembly revealed a total of 18,286 and 22,458 transcripts for C. flexuosus and C. winterianus, respectively. Furthermore, the reads were mapped against the genomes of related species, including Andropogon gerardii, Sorghum bicolor, Saccharum officinarum, Miscanthus sinensis, Miscanthus lutarioriparius, and Zea mays, to assess their conservation across these genomes. The results indicated which species are more closely related to the Cymbopogon genus and highlighted key differences in metabolic pathways.

sample_organism:
Cymbopogon flexuosus
Cymbopogon winterianus

overall_design: Two samples of leaves per species (cf1, cf2, cw1, and cw2) were used to extract total RNA and to perform sequencing.

first: Luciano

middle: C

last: da Maia

first: Antonio

last: de Oliveira

first: Camila

last: Pegoraro

first: Leticia

last: Benitez

first: Cesar

middle: V

last: Rombaldi

middle: W

last: Arge

first: Eugenia

last: Braga


title: scHiCAR: a tri-modal single-cell genomics technology for integrated transcriptome, epigenome, and 3D genome analysis in complex tissues [mouse_brain_scHiCAR_1]

city: Durham

first: Yarui

last: Diao

address: 307 Research Drive

department: Cell Biology

institute: Duke University

summary: The three-dimensional (3D) organization of cis-regulatory elements (CREs) plays a central role in transcription control. However, capturing transcriptome, epigenome, and 3D genome from the same single cells remains technically challenging. Here, we present scHiCAR (single-cell Hi-C with ATAC and RNA-seq), a combinatorial barcoding-based method that simultaneously profiles mRNA, open chromatin, and chromosome-conformation-capture from the same cells. Compared to existing single-cell 3D genome methods, scHiCAR more efficiently enriches long-range cis-interactions anchored at candidate CREs (cCREs). Applied to 1.62 million mouse brain cells and complemented with a deep learning-based loop caller, scHiCAR accurately defines cell-type-specific transcriptomes, accessible cCREs, and 5kb-resolution enhancer-promoter pairs across 22 brain cell types. scHiCAR also performs robustly in challenging tissues such as skeletal muscle, enabling tri-modal single-cell level analysis of gene regulation dynamics during muscle stem cell regeneration. scHiCAR offers a scalable, efficient, and cost-effective platform for studying gene regulatory landscapes in complex tissues at single-cell resolution.

overall_design: To evaluate scHiCAR’s performance in complex tissues, we selected the mouse frontal cortex due to its complex cellular diversity and the availability of high-quality single-cell reference datasets for benchmarking.

first: Xiaolin

last: Wei

first: Yueyuan

last: Xu

first: Dongchan

last: Yang


title: Normalizing body weight with a dietary strategy mitigates obesity-accelerated pancreatic carcinogenesis in mice

city: Davis

first: Gerardo

last: Mackenzie

state: California

address: 1 Shields Ave

institute: University of California Davis

summary: Although obesity is a modifiable risk factor for pancreatic cancer, the role of dietary changes that lead to weight loss in pancreatic carcinogenesis remains unknown. Thus, we determined the effects of weight normalization via dietary switch on pancreatic carcinogenesis and the associated mechanisms. Five-week-old male and female LSL-KrasG12D/+; p48Cre/+ (KC) mice (8-12/diet group/sex) were fed a high-fat, diet-induced obesity diet (DIO; 60 kCal% energy from fat) or a low-fat, control diet (CD; 11 kCal% energy from fat) for 21 weeks. A subset of mice was fed the DIO for 8 weeks, then switched to a CD for 13 additional weeks (DIO→CD). Cancer incidence was evaluated by histology. Lipidomics and RNAseq followed by bioinformatic analysis were conducted to identify possible mechanisms. The gut microbiome was characterized using 16s rRNA amplicon sequencing. After 21 weeks, DIO-fed mice had significantly higher body weight, fat mass, and pancreatic acinar-to-ductal metaplasia compared to the other 2 groups.  While none of the 21 mice fed a CD developed cancer, 2 out of 21 DIO-fed mice did. Switching from a DIO to a CD normalized body weight and composition, reduced acinar-to-ductal metaplasia and prevented cancer incidence with no mice developing cancer. Mechanistically, the DIO affected the expression of genes regulating cellular metabolism, immune function, and cell-signaling, while CD and DIO→CD had similar global gene expression. Moreover, DIO increased epoxy metabolites of linoleic acid, which were mitigated by the dietary switch. Finally, compared to a CD, DIO altered the gut microbiome and switching from a DIO to a CD restored the gut microbiome profile to one close to the mice fed a CD. Body weight normalization mitigates obesity-accelerated pancreatic carcinogenesis, in part, by affecting inflammatory and cell signaling pathways, reducing epoxy metabolites, and modulating the gut microbiome.

overall_design: RNA-seq of the pancreas from female LSL-KrasG12D/+; p48Cre/+ (KC) mice fed either: 1) a high-fat, diet-induced obesity diet (DIO) for 21 weeks, 2) a low-fat control diet (CD) for 21 weeks, or 3) a DIO diet for 8 weeks followed by a CD diet for 13 weeks (DIO→CD).

middle: G

first: Joanna

last: Wirkus

first: Aya

last: Ead

first: Irena

last: Krga

first: Yige

last: Wang

first: Matthew

last: Pontifex

first: Michael

last: Muller

first: David

last: Vauzour

first: Karen

last: Matsukuma

first: Guodong

last: Zhang


title: Inhibition of GSK3 and TSC2 Mediates the Oncogenic Activity of AKT in Hepatocellular Carcinoma

city: Honolulu

first: Xue

state: Hawaii

address: 701 Ilalo Street

institute: University of Hawaii Cancer Center

summary: Aberrant activation of AKT is a key oncogenic driver in hepatocellular carcinoma (HCC). As AKT activates multiple downstream signaling pathways, the key mechanisms mediating AKT-driven tumorigenesis must be elucidated to develop optimal treatment strategies. Using an Akt/NRas-induced HCC mouse model, we found that AKT promotes tumorigenesis by targeting TSC2 and GSK3α&β rather than FOXO family members. Loss of either TSC2, leading to mTORC1 activation, or both GSK3 isoforms cooperated with activated NRAS to promote HCC formation in vivo, albeit with different latencies. Simultaneous TSC2 and GSK3α&β deletion cooperated with NRAS to rapidly induce HCC formation, mirroring observations from the Akt/NRas HCC model. RNA-seq studies indicated distinct pathways regulated by TSC2/mTORC1 and GSK3α&β during hepatocarcinogenesis, with FOXM1 functioning as a major effector of GSK3. In summary, these findings uncover AKT’s role in suppressing the TSC complex and GSK3 to drive HCC, offering mechanistic insights into oncogenic signaling and potential therapeutic targets.

overall_design: RNA-seq profiling of normal liver (NL) and liver tumors from murine HCC models induced by Akt/Nras and Akt/Nras/Foxo1AAA.

first: Xin

last: Chen

first: Guofei

last: Cui


title: Therapeutic Strategies for MMAE-Resistant Bladder Cancer Through DPP4 Inhibition

city: Kagoshima

first: Gang

last: Li

address: 8-35-1 Sakuragaoka

department: Urology

institute: Graduate School of Medical and Dental Sciences, Kagoshima University

summary: Monomethyl auristatin E (MMAE) is used as the cytotoxic payload for enfortumab vedotin (EV) in the treatment of locally advanced and metastatic bladder cancer (BC). However, the development of resistance to MMAE in BC is a therapeutic problem. To explore the mechanism of resistance to MMAE in BC, we established MMAE-resistant BC cells (MR-BCs). RNA sequencing analysis showed that the expression of dipeptidyl peptidase 4 (DPP4, also called CD26) increased significantly in MR-BCs compared with parental BC cells. Knock down of DPP4 expression using small interfering RNA inhibited the viability of MR-BCs. In addition, the DPP4 inhibitor sitagliptin suppressed the proliferation, migration, and invasion of BC cells, and cotreatment with MMAE effectively induced cell apoptosis, arrested cells in the G2M phase of the cell cycle, increased reactive oxygen species production by inhibiting the AKT pathway, and significantly inhibited the in vivo growth of MMAE-resistant cells. This study provides insights into the use of DPP4 inhibitors as a treatment strategy for MMAE-resistant BC.

overall_design: We established MMAE-resistant BC cells, MMAE-resistant T24 (MR-T24) and MMAE-resistant J82 (MR-J82). Then, we performed RNA sequencing analysis to compare gene expression levels between MR-T24 and T24, as well as MR-J82 and J82.


title: The transcriptional differences between mCAR-T and cmCAR-T cells

city: shanghai

first: kaicheng

last: Zhou

state: shanghai

address: Jinke road 3728

department: Pharmacy school

institute: Fudan University

summary: The study investigates the transcriptional differences between mCAR-T and cmCAR-T cells to understand their distinct cell-killing and cytokine release behaviors. RNA-seq experiments revealed that untransfected T cells, cmCAR-T, and mCAR-T cells exhibit significant transcriptomic differences on days 2 and 4. Notably, the GZMB gene, associated with cytotoxicity, was expressed at higher levels in cmCAR-T cells compared to mCAR-T cells. Analysis of gene signatures related to T cell activation and exhaustion showed distinct patterns between the two cell types. Differentially expressed genes (DEGs) highlighted enriched cytokine signaling in cmCAR-T cells on day 2 and interferon signaling on day 4. These findings suggest that while both CAR-T cell types have transient functional signals, cmCAR-T cells demonstrate enhanced and prolonged cytotoxicity compared to mCAR-T cells.

overall_design: Control T cells (untransfected), Linear mRNA CAR-T or cmRNA CAR-T cells (n=3) were harvested at day 2 and day 4 post electroporation transfections. Subsequently, the total RNA was extracted from cell samples using TRIzol Reagent (Thermo Fisher Scientific, 15596026CN) for preparing RNA libraries using the VVAHTS® Universal V8 RNA-seq Library Prep Kit for Illumina (Vazyme, NR605-0). Sequencing was performed using the Illumina NovaSeq 6000 platform.

first: Qinchao

last: Hu

first: Hui

last: Zhao

first: Kaicheng

first: Xuyao


title: Targeting FOXA1 and FOXA2 Disrupts the Lineage-Specific Oncogenic Output in Prostate Cancer [ChIP-seq]

city: Bellinzona

first: Jean-Philippe

last: Theurillat

address: Via Francesco Chiesa 5

institute: Institute of Oncology Research

summary: Activation of the androgen receptor (AR) is the key lineage-specific oncogenic pathway and the primary therapeutic target in prostate cancer. While AR signaling is enabled by the pioneer transcription factor FOXA1, its homologue FOXA2 is specifically expressed in advanced lineage plasticity prostate cancers that have lost the AR signaling axis. However, their roles and utility as a drug target remain incompletely characterized. Here, we show an unexpected collaboration of FOXA1 and FOXA2 in mediating AR-independent cell proliferation in different lineage plasticity cancer subtypes. Conversely, joint loss-of-function or pharmacologic disruption of FOXA1 and FOXA2 leads to the collapse of lineage-specific oncogenic transcription factors followed by cell cycle arrest. In summary, our findings uncover a druggable dependency for AR-positive and -negative prostate cancers.

overall_design: To investigate the role of FOXA1 and FOXA2 in CRPCs, we used different prostate cancer cell lines LNCaP in the context of AR inhibition, FOXA2 over expression and PC3 for double knock down of FOXA1 and FOXA2 and a small compound T treatment.

first: Nicolo

last: Formaggio

first: Gayathri

last: Thillaiyampalam

first: Claudio

last: Lorenzi

first: Andrea

last: Rinaldi


title: Ectopic expression of a deletion variant of cystathionine gamma-synthase 2 (GmCGS2) in soybean increases expression of genes encoding sulfur amino acid-rich proteins

city: Indianapolis

first: Shreedharan

last: Sriram

state: IN

address: 9330 Zionsville Rd

institute: Corteva Agriscience

summary: A deletion variant of GmCGS2 was ectopically expressed in soybean with a diverse range of expression levels and patterns. A combination of a soybean ubiquitin promoter and an in-frame deletion in GmCGS2, from K66 to S143, resulted in increased seed Met and Cys contents without incurring a yield penalty in a ten-location field trial. Transgenic events of this construct had increases of 41 to 114%, 10 to 12%, and 4.7 to 7.3% in free Met, total Cys, and total Met, respectively. RNAseq analysis of developing seed revealed increased transcript for three Cys-rich Bowman-Birk protease inhibitor (BBI) genes, and for two Met-rich 2S albumin genes, with little effect apparent on genes of primary sulfur metabolism. Trypsin-agarose chromatography, protease inhibition assays, and mass spectrometry analysis revealed increased BBI and 2S albumin proteins. The additional BBI protein was determined to be 1.5 to 1.8% of the protein in transgenic seed, sufficient to account for the increased Cys content. The observation that overexpressing an enzyme involved in Met biosynthesis that used Cys as a substrate still increased total Cys more than total Met suggested a lack of native Met-rich soybean proteins capable of incorporating the additional free Met.

overall_design: RNAseq analysis of developing seed was done for transgenic events e15 and e19 of the GmUBQ promoter construct compared to nulls.

first: Keith

last: Roesler

first: Kayla

middle: S

last: Flyckt

first: Laura

last: Wayne


title: Targeting FOXA1 and FOXA2 Disrupts the Lineage-Specific Oncogenic Output in Prostate Cancer [RNA-seq]

overall_design: To investigate the role of FOXA1 and FOXA2 in CRPCs, we used different prostate cancer cell lines LNCaP in the context of AR inhibitionand and PC3 for double knock down of FOXA1 and FOXA2  and a small compound T treatment.


title: Self-tolerance maintained by self-reactive CD8+ T cells

city: hangzhou

first: wang

last: pengfei

address: yuhangtang road 866

institute: zhejiang university

summary: CD8+ T cells play a critical role in immune tolerance maintainnance after immune activation. It is known to function through targeting activated CD4+ T cells, in both Qa-1- and MHC-Ia-restricted9 manner. However, the exact nature of this targeting process, i.e., the specific peptides and the corresponding reactive CD8 TCRs, remains unknown. In this study, we identified the self-peptides on activated CD4+ T cells that could mediate the CD8+ T cells immunosuppressive activity. By cloning the corresponding CD8 TCRs and the generation of TCR transgenic mice , we were able to validate the immunosuppressive function of CD8+ T cells carrying the self-reactive TCRs both in vitro and in vivo. The therapeutic potential of peptide vaccination and CD8+ T cell transfer were confirmed in a mouse EAE model. This study suggest that self-tolerance can be maintained by self-reactive CD8+ T cells recognizing self-antigenic peptides through specific TCRs, thus redefine the nature of CD8+ regulatory T cells as self-reactive CD8+ T cells.

overall_design: To investigate the transcriptomic characteristics and TCR clonotypes of self-antigen-specific CD8 T cells, we performed single-cell RNA sequencing and TCR sequencing on CD8 T cells stimulated with self-antigens.

first: Yadan

last: Bai

first: Pengfei

last: Wang

first: Fan

first: Linrong

last: Lu


title: Mechanisms Underlying Morphological and Functional Changes of Cilia in Fibroblasts Derived from Patients Bearing ARL3T31A and ARL3T31A/C118F Mutations

city: zhengzhou

first: xiaoli

last: zhang

address: 河南省郑州市二七区连云路15号院11号楼29号

institute: zhengzhou university

summary: ARL3 plays a crucial role in cilia development, while mutations in ARL3 are closely associated with ciliopathies. In a previous study, we reported distinct phenotypes of retinal dystrophy in patients with single ARL3T31A and compound ARL3T31A/C118F mutations, indicating that different mutation types may exert diverse effects on their functions. Here, we generated fibroblasts from patients carrying single ARL3T31A and compound ARL3T31A/C118F mutations, systematically evaluated their cilia morphology and function, and explored the underlying molecular mechanisms by RNA-sequencing. Our results showed that both ARL3T31A and ARL3T31A/C118F mutations led to a decrease in cilia incidence. The compound ARL3T31A/C118F mutations caused significantly elongated cilia and impaired retrograde transport, whereas the single ARL3T31A mutation did not induce significant changes in fibroblasts. Compared to ARL3T31A, ARL3T31A/C118F fibroblasts exhibited a higher enrichment of biological processes related to neuron projection development, tissue morphogenesis, and extracellular matrix (ECM) organization, with noticeable alterations in pathways such as ECM-receptor interaction, focal adhesion, axon guidance, and TGF-β signaling. Core regulated genes including IQUB, UNC13D, RAB3IP, and GRIP1 were specifically downregulated in the ARL3T31A/C118F group, which were further validated. Additionally, we observed that IQUB had a rescuing effect on the overlong cilia observed in ARL3T31A/C118F fibroblasts. These findings suggest that the ARL3T31A/C118F mutation downregulates IQUB, disrupting TGF-β signaling cascades and leading to cilia elongation in ARL3T31A/C118F cells. Our results not only enhance our understanding of ARL3-related diseases but also provide new insights into the analysis of single and compound mutations in genetics.

overall_design: we generated control and patient immortal skin fibroblast and conducted RNA-seq, and compare differential expressed genes in control and patient RNA-seq data.

first: shun

last: yao

first: bo

last: lei

first: xiuxiu

last: jin


title: Targeting FOXA1 and FOXA2 Disrupts the Lineage-Specific Oncogenic Output in Prostate Cancer

first: Jean-Philippe

last: Theurillat

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: KDM5A epigenetically orchestrates MHC-I associated anti-tumor immunity of immunotherapy [tumor-CUTTag]

city: Beijing

first: Tantan

address: Haidian  District

institute: Tsinghua University

summary: Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Histone methylation was involved in anti-tumor immunity of ICB. However, the link between histone methylation and MHC-I regulation and the related mechanisms are poorly understood. Here we show that KDM5A, an H3K4 demethylase that is critical for MHC-I expression and associated antigen presentation capacity, induces robust immune response and enhances ICB efficacy. Mechanistically, KDM5A upregulates IFN-gamma/STAT1-mediated MHC-I expression via directly binding and suppressing Scos1 in tumor cells. The genes encoding the lysosomal cathepsins are recognized and up-regulated by KDM5A, resulting in enhanced antigen-presentation abilities of both tumor cells and dendritic cells. Furthermore, pharmacological enhancing KDM5A improves response to anti-PD-1 therapy. These investigations demonstrate that enhancing KDM5A triggers MHC-associated antigen presentation of both tumor cells and DCs simultaneously to boost antitumor immunity, thus represents a candidate ICB sensitizer.

overall_design: CUT&Tag for the mouse  B16-OVA cells and cDC1s were carried out using a KDM5A specific antibody to map direct targets bound by KDM5A.

first: Dan

last: Li


title: Hyperactive lateral habenula mediates the comorbidity between rheumatoid arthritis and depression-like behaviors

city: Guangzhou

first: Wenchang

address: No. 78, Zhongshan 2nd Road

institute: The Fifth Affiliated Hospital of Sun Yat-sen University

summary: Objective: The aim of this study was to identify the neural and molecular mechanisms underlying the comorbidity of rheumatoid arthritis (RA) and depression. Methods: A cohort of 200 RA patients were recruited to quantitatively assess the association between depressive symptoms and RA disease activity, as well as quality of life. The collagen antibody-induced arthritis (CAIA) mouse model of RA was used to screen for brain regions that showed changes in c-FOS expression, an indicator of alteration in brain activity, accompanying the appearance of depression-like behaviors. RNA sequencing, immunostaining, AAV-mediated expression, micro-CT, plasma cytokines/chemokines measurements and histological analyses were applied to evaluate the contribution of the identified brain region in the disease progression of RA and depression-like symptoms. Results: In this study, we showed that in RA patients, the depression scores were significantly correlated with the severity and quality of life of the patients. The CAIA mice developed RA symptoms, together with depression-like behaviors accompanied by hyperactivity and alterations in gene expression reflecting cerebrovascular disruption in the lateral habenula (LHb), a brain region processing negative valence. Importantly, inhibition of the LHb outputs not only alleviated depression-like behaviors, but also resulted in rapid remission of RA symptoms and reduction in sympathetic nerve fibers in the synovial joints of the CAIA mice.Conclusion: Our study highlights a critical but previously overlooked contribution of hyperactive LHb to the comorbidity between RA and depression, suggesting that targeting LHb in conjunction with RA treatments may be a promising strategy for RA patients comorbid with depression.

overall_design: This study explores the relationship between RA and depression by investigating the self-reported behavior of RA patients. And further explore the molecular mechanism of RA comorbidity depression through animal models.

first: Peihui

last: Wu

first: Rongke

last: Lv

first: Wenbao

last: Cai

last: Lian

first: Bizhen

last: Ke

first: Xin

last: Cheng

first: Yubo

last: Hu

first: Yi

last: Chen

first: Zaohui

last: Ma

first: Meiqi

first: Weiping

last: Dai

first: Pei

last: Xia

first: Yangyang

last: Lin

first: Weijie

first: Xiaojing

last: Ye


title: KDM5A epigenetically orchestrates MHC-I associated anti-tumor immunity of immunotherapy [DC-CUTTag]

first: Tantan

last: Wang


title: Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays [60min]

status: Public on Aug 29 2025

city: Cambridge

first: Ritu

last: Raman

state: MA

address: 77 Massachusetts Avenue

department: Mechanical Engineering

institute: Massachusetts Institute of Technology

summary: Exercise has long been considered an essential part of human health and longevity. Recent physiological studies have expanded muscle’s role beyond simply acting as an actuator, revealing muscle’s exercise-mediated paracrine and endocrine relationships with other organ systems. In vitro engineered skeletal muscle models can address physiological questions about exercise adaptation with the precision of cell biology. Optogenetic tools have enabled a noninvasive approach to stimulating muscle contraction that avoids the potential off-target effects of electrical stimulation techniques. In this article we propose high-throughput culture and optical exercise protocols to generate statistically robust cellular exercise response datasets. We characterize optical rheobase for 2D muscle tissue morphology, finding that optical intensities as low as 5 μW mm-2 can trigger contraction. We then analyze bulk RNA sequencing data collected from high throughput, acute exercise protocols and find a rich display of transcriptional behavior that is consistent with experimental observations. The spontaneous contractility of our tissue constructs introduced oxygen diffusion challenges when maintained in a 24 well plate, and our analysis shows divergent myogenic and pathological transcriptional consequences of hypoxia. We believe our techniques provide a practical foundation for conducting future high-precision in vitro exercise studies of skeletal muscle.

overall_design: ChR2 C2C12 myoblasts (optogenetic) grown on a fibrin hydrogel and differentiated for about two weeks before RNA extraction. This cohort underwent daily optical stimulation for 60 minutes at a variety of frequencies (none-control, 1Hz, 4Hz, and 10Hz).

first: Ronald

last: Heisser

first: Angel

last: Bu


title: Extracellular matrix-myCAF signatures correlate with resistance to neoadjuvant aPD-L1 immune checkpoint inhibition with durvalumab + metformin in HPV+ HNSCC

city: Philadelphia

first: Alban

last: Linnenbach

state: PA

address: 233 S. 10th Street, Building BLSB 412

department: Kimmel Cancer Center

institute: Thomas Jefferson University

summary: In HPV-positive head and neck squamous cell carcinoma (HNSCC), early resistance to neoadjuvant durvalumab plus metformin therapy is associated with baseline enrichment of extracellular matrix–associated myofibroblastic cancer-associated fibroblasts (ECM-myCAF) within the tumor compartment. In contrast, treatment responders exhibit a distinct tumor microenvironment marked by baseline enrichment of Langerhans-like dendritic cells and post-treatment upregulation of antigen presentation pathways. These findings highlight the tumor-stroma interface as a key determinant of immunotherapy response and provide a foundation for biomarker-driven patient selection. Identifying stromal and immune signatures predictive of response to neoadjuvant aPD-L1 therapy supports future strategies targeting the tumor microenvironment to improve outcomes in HNSCC.

overall_design: Unbiased GSEA

first: Pablo

last: Llerena

first: Hani

last: Samarah

first: Kathryn

last: Nunes

first: Zhao

first: Kelly

last: Bridgham

first: Sruti

last: Tekumalla

first: Amiti

last: Jain

first: Larry

last: Harshyne

first: Sanket

last: Shukla

first: Ioannis

last: Vathiotis

first: Madalina

last: Tuluc

first: Stacey

middle: M

last: Gargano

first: John

middle: R

last: Eisenbrey

first: Scott

last: Keith

first: David

last: Cognetti

first: Voichita

last: Bar-Ad

first: Adam

last: Luginbuhl

first: Rita

last: Axelrod

first: Rajanikanth

last: Vadigepalli

first: Hushan

last: Yang

first: Diana

last: Whitaker-Menezes

first: Megan

last: Roche

first: My

last: Mahoney

first: Athanassios

last: Argiris

first: Charalambos

last: Solomides

first: Jennifer

last: Johnson

first: Mouadh

last: Barbirou

first: Amanda

last: Miller

first: Andrew

last: South

first: Ramkrishna

last: Mitra

first: Ubaldo

last: Martinez-Outschoorn

first: Joseph

last: Curry