虎杖苷通过抑制miR-301a促进胃癌SGC-7901细胞凋亡的机制研究

Study on the Mechanism of Polydatin Promotes Apoptosis of Gastric Cancer SGC-7901 Cells by Inhibiting miR-301a

目的:探究虎杖苷通过miR-301a表达调节进而促进胃癌SGC-7901细胞凋亡的作用机制。方法:通过qRT-PCR检测虎杖苷处理后胃癌SGC-7901细胞中miR-301a的表达及miR-301a mimics在细胞中转染后的转染效率;通过CCK8法检测细胞增殖能力;流式细胞术检测细胞凋亡情况;Western blotting检测相关凋亡蛋白的表达情况。结果:与对照组比较,虎杖苷处理后能够抑制胃癌SGC-7901细胞增殖,促进凋亡(P<0.05);miR-301a过表达可以逆转虎杖苷对胃癌SGC-7901细胞增殖的抑制作用及细胞凋亡的促进作用(P<0.05);miR-301a过表达可以逆转虎杖苷对胃癌SGC-7901细胞凋亡中相关凋亡蛋白的调节作用(P<0.05)。结论:虎杖苷能够通过抑制miR-301a表达进而抑制胃癌SGC-7901细胞的增殖能力,促进细胞凋亡。

Objective:To explore the mechanism of polydatin promotes the apoptosis of gastric cancer SGC-7901 cells by regulating the expression of miR-301 a.Methods:The expression of miR-301 a in gastric cancer SGC-7901 cells and the transfection efficiency of miR-301 a mimics were determined by qRT-PCR.The cell proliferation ability was detected by CCK-8 assay.Flow cytometry was used to detect cell apoptosis.Western blotting was used to detect the expression of related apoptotic proteins.Results:Compared with the control group,polydatin can inhibit the proliferation and promote apoptosis of gastric cancer SGC-7901 cells(P<0.05).Overexpression of miR-301 a could reverse the inhibitory effect of polydatin on the proliferation of gastric cancer SGC-7901 cells and the promotion of apoptosis(P<0.05).Overexpression of miR-301 a could reverse the regulation of polydatin on apoptosis related apoptosis proteins in gastric cancer SGC-7901 cells(P<0.05).Conclusion:Polydatin can inhibit the proliferation of gastric cancer SGC-7901 cells and promote cell apoptosis by inhibiting the expression of miR-301 a.