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机构地区:[1]广州市红十字会医院检验科,广东广州510220 [2]广州医科大学附属第二医院检验科,广东广州510260
出 处:《海南医学》2017年第7期1038-1040,共3页Hainan Medical Journal
基 金:广东省广州市科技和信息化局项目(编号:2014J4100063)
摘 要:目的探讨miR-105对人肝癌细胞增殖的影响及可能机制。方法改变QGY-7703及Hep G2两种细胞的miR-105表达,细胞克隆形成实验和软琼脂增殖试验检测细胞增殖能力的改变;流式细胞仪检测细胞周期改变。结果细胞克隆形成和软琼脂增殖实验显示,过表达miR-105可抑制QGY-7703及Hep G2细胞增殖,反之抑制miR-105表达则促进细胞增殖;细胞流式检测显示miR-105过表达能促进两种癌细胞G0/G1期阻滞。结论 miR-105抑制肝癌细胞增殖,其机制与引起细胞周期阻滞有关。Objective To investigate the effects of miR-105 expression on the proliferation of human hepatocellular carcinoma(HCC) cells. Methods Over-expression of miR-105 was transfected by miR-105 mimics, and inhibition of miR-105 expression was transfected by miR-105 inhibitors. The effects of miR-105 expression on the proliferation of QGY-7703 and HepG2 cells were detected by colony formation assay and soft agar proliferation experiment.Flow cytometry was used to examine the influence of miR-105 expression on the cell cycle distribution of HCC cells.Results Colony formation assay and soft agar proliferation experiment showed that, the proliferation of QGY-7703 and HepG2 cells were suppressed by miR-105 over-expression(P〈0.05), while miR-105 inhibitor accelerated the proliferation of HCC cells. The G0/G1 phase cells dramatically increased in the miR-105 over-expressing QGY-7703 and HepG2 cells, while decreased in miR-105-inhibited cells. Conclusion Mi R-105 inhibits the proliferation of HCC cells. The mechanisms may be related to the cell cycle arrested.
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