下调SMAD1表达诱导胃癌细胞周期进展及促进细胞增殖抑制细胞凋亡的作用

目的:探讨下调SMAD1表达对胃癌细胞周期、增殖及凋亡的影响。方法:将胃癌BGC-823细胞分为三组，以转染SMAD1 siRNA的细胞为SMAD1 siRNA组，转染SMAD1 control细胞为SMAD1 NC组，对照组不做任何处理。采用Western blot检测细胞的转染效果及PTEN、Bcl-xL 和p21蛋白的表达情况，CCK-8法检测细胞的增殖情况，流式细胞仪检测细胞周期变化和细胞凋亡率。结果:转染48 h后，SMAD1 siRNA组细胞中SMAD1蛋白的相对表达量显著降低（P＜0.05）；细胞在G0/G1期所占比例显著降低，S期所占比例显著升高；SMAD1 siRNA组细胞的OD值、Bcl-xL蛋白的相对表达量显著升高，而细胞凋亡率及PTEN、p21蛋白的相对表达量显著降低，差异均有统计学意义（P＜0.05）。结论:下调SMAD1表达能够诱导BGC-823细胞从G0/G1期进入S期，促进细胞增殖并抑制细胞凋亡，其作用机制可能与下调PTEN、p21蛋白表达及上调Bcl-xL蛋白表达有关。

Down-regulation of SMAD1 expression induces cell cycle progression,promotes cell proliferation and inhibits apoptosis in gastric cancer cells

Objective:To investigate the effect of down-regulation of SMAD1 expression on cell cycle,proliferation and apoptosis in gastric cancer cells.Methods:Gastric cancer BGC-823 cells were divided into three groups,and the cells transfected with SMAD1 siRNA were SMAD1 siRNA group,transfected with SMAD1 control cells as SMAD1 NC group,and the control group did not do any treatment.The transfection effect and the expression of PTEN,Bcl-xL and p21 protein were detected by Western blot.The proliferation of cells was detected by CCK-8 assay,and the cell cycle and apoptosis rate were detected by flow cytometry.Results:After transfection with 48 h,the relative expression of SMAD1 protein in SMAD1 siRNA group was significantly decreased.The proportion of cells in G0/G1 phase decreased significantly,and the proportion of S cells increased significantly.The OD value of the cells and the relative expression of Bcl-xL protein in SMAD1 siRNA group increased significantly.The apoptosis rate and the relative expression of PTEN and p21 protein were significantly decreased,which differences were statistically significant (P＜0.05).Conclusion:Down-regulation of SMAD1 expression can induce BGC-823 cells to enter S phase from G0/G1 phase,and promote cell proliferation and inhibit cell apoptosis,and its mechanism may be related to down-regulating the expression of PTEN and p21 protein and up-regulating the expression of Bcl-xL protein.