敲低PRMT5基因表达对胃癌细胞增殖、侵袭和凋亡的影响及其机制

Effect of PRMT5 Expression Knockdown on Proliferation,Invasion and Apoptosis of Gastric Cancer Cells and Its Mechanism

目的观察蛋白质精氨酸甲基转移酶5(PRMT5)在胃癌细胞中的表达,探讨敲低PRMT5表达水平后对胃癌细胞生物学行为的影响。方法Western blot检测胃癌细胞系MGC803、SGC7901、MKN45和人胃黏膜上皮细胞GES-1中PRMT5蛋白表达水平,转染siRNA1和siRNA2质粒敲低PRMT5的表达水平,细胞增殖和凋亡实验、Transwell实验分别检测细胞增殖能力、凋亡率和细胞的侵袭能力,Western blot检测β-catenin、Cyclin D1和Bax蛋白表达水平。结果与GES-1细胞比较,MGC803、SGC7901和MKN45细胞中PRMT5蛋白表达水平增加(P<0.001)。敲低PRMT5表达后细胞的增殖和侵袭能力减弱,凋亡率增加(P<0.05),β-catenin和Cyclin D1蛋白的表达降低,Bax蛋白的表达增加(P<0.001)。结论PRMT5在胃癌细胞中表达水平升高,敲低其表达水平后可通过减弱Wnt/β-catenin信号通路转导抑制细胞的增殖和侵袭并促进细胞凋亡。

Objective To observe the expression level of PRMT5 in gastric cancer cells,and explore the effect of knocking down the expression level of PRMT5 on the biological behavior of gastric cancer cells.Methods Western blot was used to detect the expression of PRMT5 protein in gastric cancer cell lines MGC803,SGC7901,MKN45 and human gastric epithelial cells GES-1.siRNA1 and siRNA2 plasmids were transfected to knock down the expression of PRMT5.Cell proliferation and apoptosis assay,transwell assay were used to detect cell proliferation,apoptosis and invasion abilities,respectively.The protein expression levels of β-catenin,cyclin D1 and Bax were detected.Results Compared with GES-1 cells,PRMT5 protein expression levels increased in MGC803,SGC7901 and MKN45 cells(P<0.001).After knocking down the expression of PRMT5,the cell proliferation and invasion abilities were weakened,the apoptosis rate increased(P<0.05),the expression of β-catenin and Cyclin D1 protein decreased,and the expression of Bax protein increased(P<0.001).Conclusion The expression level of PRMT5 is increased in gastric cancer cells.Knockdown of PRMT5 expression level could inhibit cell proliferation,invasion and promote cell apoptosis via reducing Wnt/β-catenin signaling pathway.