miR-210通过NF-κB信号通路对胃癌细胞的增殖、凋亡、侵袭及转移的影响

Effects of miR-210 via NF-κB signaling pathway on the proliferation,apoptosis,invasion,and metastasis of gastric cancer cells

目的 研究miR-210通过核转录因子(NF-κB)信号通路对胃癌细胞的增殖、凋亡、侵袭和转移的影响。方法 使用qRT-PCR检测并比较正常胃黏膜上皮细胞和MGC803胃癌细胞中miR-210的表达水平,根据不同的处理方式,将胃癌细胞分为空白对照组、阴性对照组(miR-210 inhibitor control)及实验组(miR-210 inhibitor),使用qRT-PCR检测各组细胞中miR-210水平,比较转染后各组细胞的增殖、凋亡、侵袭和迁移情况,比较各组细胞中人核因子κB抑制蛋白α(IκBα)、磷酸化-人核因子κB抑制蛋白α(p-IκBα)、NF-κB、磷酸化核转录因子(p-NF-κB)蛋白水平。结果 与正常胃黏膜上皮细胞相比,MGC803胃癌细胞中miR-210水平升高(P<0.05);与空白对照组和阴性对照组细胞相比,实验组细胞中miR-210表达水平、细胞增殖能力、侵袭和迁移能力均降低,细胞凋亡率升高(P<0.05),实验组细胞中IκBα、p-IκBα、NF-κB和p-NF-κB蛋白水平均降低,差异均有统计学意义(P<0.05)。结论 MGC803胃癌细胞内miR-210的表达明显升高,miR-210可通过抑制NF-κB信号通路抑制胃癌细胞增殖、侵袭和迁移,并促进胃癌细胞凋亡。

Objective To investigate the effects of miR-210 via nuclear factor kappa-B(NF-κB)signaling pathway on the proliferation,apoptosis,invasion and metastasis of gastric cancer cells.Method qRT-PCR test was used to detect and compare expression of miR-210 in normal gastric mucosal epithelial cells and MGC803 gastric cancer cells.According to processing differences,gastric cancer cells were divided into blank control group,negative control group(miR-210 inhibitor control)and experimental group(miR-210 inhibitor).The proliferation,apoptosis,invasion and metastasis after transfection were compared by qRT-PCR tested miR-210 levels in all groups;and protein levels of IκBα,p-IκBα,NF-κB,and p-NF-κB in each group were compared.Results Compared with normal gastric mucosal epithelial cells,the levels of miR-210 in MGC803 gastric cancer cells increased(P<0.05).Compared with the blank control group and negative control group,the experimental group showed a decrease in miR-210 expression,cell proliferation ability,invasion and metastasis ability,but an increase in cell apoptosis rate(P<0.05),IκBα,p-IκBα,NF-κB,and p-NF-κB protein levels all decreased,differences were statistically significant(P<0.05).Conclusion Expression of miR-210 increases significantly in MGC803 gastric cancer cells.miR-210 can inhibit the proliferation,invasion,and metastasis of gastric cancer cells and promote gastric cancer cell apoptosis by inhibiting the NF-κB signaling pathway.