miR-155对喉鳞状细胞癌Hep2细胞增殖影响及机制

发布时间：2018-03-08 10:46

本文选题：miR-　切入点：喉鳞状细胞癌　出处：《中国公共卫生》2017年07期 　论文类型：期刊论文

【摘要】：目的探讨miR-155对喉鳞状细胞癌Hep2细胞增殖影响及具体机制。方法采用miR-155 NC和miR-155 inhibitor转染Hep2细胞,realtime-PCR法检测转染效果,细胞计数盒-8(CCK-8)法检测不同转染时间(12、24、36、48、60、72 h)细胞活力,流式细胞术检测细胞凋亡及细胞周期;Western blot检测Hep2细胞中细胞周期蛋白A1(cyclin A1)、cyclin D1、磷脂酰肌醇3激酶/蛋白激酶B/叉形头转录因子(Foxo3a)信号通路相关蛋白表达量。结果 miR-155 inhibitor组中miR-155表达量(0.34±0.03)明显低于miR-155 NC组(1.25±0.10),且转染24、36、48、60、72 h后,miR-155 inhibitor组Hep2细胞活力明显低于miR-155 NC组;与miR-155 NC组比较,miR-155 inhibitor组Hep2细胞凋亡率明显提高,细胞周期阻滞于G1期,cyclin A1、cyclin D1、PI3K、p-AKT表达下调,Foxo3a表达上调,差异均有统计学意义(均P0.01)。结论 miR-155表达下调可降低Hep2细胞活力、增加细胞凋亡率,其机制可能与miR-155调控PI3K/AKT/Foxo3a信号通路有关。
[Abstract]:Objective to investigate the effect of miR-155 on the proliferation of Hep2 cells in laryngeal squamous cell carcinoma (LSCC) and its specific mechanism. Methods the transfection effect was detected by miR-155 NC and miR-155 inhibitor transfection of Hep2 cells by realtime-PCR, and the viability of Hep2 cells at different transfection times was detected by cell count box (CCK-8) assay. Flow cytometry was used to detect cell apoptosis and cell cycle blot was used to detect the expression of cyclin D1, phosphatidylinositol 3 kinase / protein kinase B / fork head transcription factor Foxo3a in Hep2 cells. The expression of miR-155 in miR-155 inhibitor group was significantly lower than that in miR-155 NC group (0.34 卤0.03), and the activity of Hep2 cells in MIR-155 inhibitor group was significantly lower than that in miR-155 NC group. Compared with miR-155 NC group, the apoptosis rate of Hep2 cells was significantly increased, and the cell cycle was blocked at G1 phase by down-regulating the expression of Foxo3a in cyclin A _ 1 cyclin D _ (1) PI3K _ (p-AKT) group (all P 0.01). Conclusion the down-regulation of miR-155 expression can decrease the activity of Hep2 cells. The mechanism of increasing apoptosis may be related to the regulation of PI3K/AKT/Foxo3a signaling pathway by miR-155.
【作者单位】：川北医学院附属医院耳鼻咽喉头颈外科;
【分类号】：R739.65

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