title: LIFRα-CT3 induces differentiation of a human acute myelogenous leukemia cell line HL-60 by suppressing miR-155 expression through the JAK/STAT pathway.
abstract: The distal cytoplasmic motifs of the leukemia inhibitory factor receptor α-chain (LIFRα-CT3) and its TAT fusion protein (TAT-CT3) can independently suppress cell viability and induce myeloid differentiation in human leukemia HL-60 cells in our previous studies. But its underlying mechanism remains undefined. Herein, we show that a prokaryotic expressed TAT-CT3 induced a rapid elevation of STAT3 phosphorylation (pSTAT3), and then suppress the transcription of miR-155 and induce the elevation of SOCS-1, which further inhibited STAT3 phosphorylation for a long-term period. Our result indicated a novel mechanism of TAT-CT3 to promote HL60 cells differentiation, which provides some potential therapeutic targets for future acute myelogenous leukemia therapy.
authors.affiliation: Department of Embryology and Histology, Second Military Medical University, Shanghai 200433, PR China.
authors.forename: Sha
authors.initials: S
authors.lastname: Xu
authors.affiliation: Department of Embryology and Histology, Second Military Medical University, Shanghai 200433, PR China.
authors.forename: Zhenyu
authors.initials: Z
authors.lastname: Xu
authors.affiliation: Graduate School, Second Military Medical University, PR China.
authors.forename: Baohai
authors.initials: B
authors.lastname: Liu
authors.affiliation: Department of Embryology and Histology, Second Military Medical University, Shanghai 200433, PR China.
authors.forename: Qing
authors.initials: Q
authors.lastname: Sun
authors.affiliation: Department of Embryology and Histology, Second Military Medical University, Shanghai 200433, PR China.
authors.forename: Ling
authors.initials: L
authors.lastname: Yang
authors.affiliation: Department of Hematology, Changhai Hospital of Shanghai, PR China.
authors.forename: Jianmin
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Embryology and Histology, Second Military Medical University, Shanghai 200433, PR China. Electronic address: wangyuesmmu@163.com.
authors.forename: Yue
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Embryology and Histology, Second Military Medical University, Shanghai 200433, PR China. Electronic address: houqiliu@126.com.
authors.forename: Houqi
authors.initials: H
authors.lastname: Liu
mesh_terms: D015153:Blotting, Western; D002454:Cell Differentiation / Q000502:physiology; D047369:Chromatin Immunoprecipitation; D005434:Flow Cytometry; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology*; D018922:HL-60 Cells; D006801:Humans; D053612:Janus Kinases / Q000378:metabolism; D053680:Leukemia Inhibitory Factor Receptor alpha Subunit / Q000235:genetics / Q000378:metabolism*; D015470:Leukemia, Myeloid, Acute / Q000235:genetics / Q000378:metabolism*; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D015514:Oncogene Proteins, Fusion / Q000235:genetics / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050791:STAT Transcription Factors / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
chemical_list: C507840:LIFR protein, human; D053680:Leukemia Inhibitory Factor Receptor alpha Subunit; C524942:MIRN155 microRNA, human; D035683:MicroRNAs; D015514:Oncogene Proteins, Fusion; D050791:STAT Transcription Factors; D053612:Janus Kinases
keywords: Acute myeloid leukemia; LIF receptor; Leukemia inhibitory factor; MicroRNA-155; Protein transduction; STAT3