ZBTB7B上调GPR17表达抑制脑胶质母细胞瘤细胞增殖OA

Objective To elucidate the transcription factor,zinc finger and BTB domain containing 7B(ZBTB7B),as a potential tumor suppressor for glioblastoma multiforme(GBM)and its molecular mechanisms,so as to provide new strategies for diagnosing and treating GBM.Methods A lentiviral vector was used to establish a U251 cell line with stable ZBTB7B overexpression.Transfection efficiency was validated via immunofluorescence,quantitative real-time polymerase chain reaction(qRT-PCR),and Western blotting(WB).Cell proliferation was assessed using live-cell dynamic monitoring,colony formation assays,and 5-bromo-2'-deoxyuridine(BrdU)incorporation assays.Rescue experiments were performed using small interfering RNA(siRNA)-mediated gene knockdown,while chromatin immunoprecipitation(ChIP)was employed to analyze the functional interaction between ZBTB7B and its downstream target,G protein-coupled receptor 17(GPR17).Results ZBTB7B overexpression significantly inhibited U251 cell proliferation(P=0.002),as evidenced by reduced colony formation(P=0.01)and BrdU incorporation(P＜0.001).Mechanistic studies revealed that ZBTB7B suppressed tumor cell proliferation by transcriptionally upregulating GPR17 expression(P＜0.001).Conclusion This study has verified the tumor-suppressive mechanism of ZBTB7B in GBM via targeted binding and regulating GPR17 expression,thus systematically elucidating its molecular mechanisms in GBM.