Retinoic acid‑incorporated glycol chitosan nanoparticles inhibit the expression of Ezh2 in U118 and U138 human glioma cells.
At present, one of the most life threatening types of adult brain tumor is glioblastoma multiforme (GBM). The molecular mechanism underlying the progression of GBM remains to be fully elucidated. The modern method of clinical treatment has only improved the average survival rates of a newly diagnosed patients with GBM by ~15 months. Therefore, the discovery of novel molecules, which are involved in glioma inhibition is required. In the present study, U118 and U138 human glioma cells were transfected with all‑trans retinoic acid (RA)-incorporated glycol chitosan (GC) nanoparticles.An MTT assay was used for the analysis of cell proliferation and flow cytometric analysis and ssDNA detection assays were performed for the determination of induction of cell apoptosis. Cell cycle distribution was analyzed by flow cytometry. Exposure of the U118 and U138 human glioma cells to the RA‑incorporated GC nanoparticles for 24 h resulted in a concentration‑dependent inhibition of cell proliferation. Among the range of experimental RA concentrations, the minimum effective treatment concentration was 10 µM, with a half maximal inhibitory concentration of 25 µM. The results also demonstrated that RA transfection resulted in the inhibition of cell proliferation, inhibition of the expression of Ezh2, and apoptosis through the mitochondrial signaling pathway by a decrease in membrane potential, the release of cytochrome c, and cell cycle arrest in the G0/G1 phase.
Department of Neurosurgery, Jingling Hospital, Clinical Medicine School of Nanjing University, Nanjing, Jiangsu 210002, P.R. China.
Hu-Chen
HC
Lu
Department of Neurosurgery, Nanjing Brain Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Jun
J
Ma
Department of Neurosurgery, Jingling Hospital, Clinical Medicine School of Nanjing University, Nanjing, Jiangsu 210002, P.R. China.
Zong
Z
Zhuang
Department of Neurosurgery, Nanjing Brain Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Yao
Y
Zhang
Department of Neurosurgery, Jingling Hospital, Clinical Medicine School of Nanjing University, Nanjing, Jiangsu 210002, P.R. China.
Hui-Lin
HL
Cheng
Department of Neurosurgery, Jingling Hospital, Clinical Medicine School of Nanjing University, Nanjing, Jiangsu 210002, P.R. China.
Ji-Xin
JX
Shi
D000328:Adult; D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D001932:Brain Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D002453:Cell Cycle / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D048271:Chitosan / Q000737:chemistry; D015536:Down-Regulation / Q000187:drug effects; D000071221:Enhancer of Zeste Homolog 2 Protein; D005909:Glioblastoma / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D006801:Humans; D053758:Nanoparticles / Q000737:chemistry*; D063151:Polycomb Repressive Complex 2 / Q000235:genetics*; D014212:Tretinoin / Q000008:administration & dosage / Q000494:pharmacology*
D000970:Antineoplastic Agents; C118638:glycol-chitosan; D014212:Tretinoin; D048271:Chitosan; C498409:EZH2 protein, human; D000071221:Enhancer of Zeste Homolog 2 Protein; D063151:Polycomb Repressive Complex 2