幽门螺杆菌VacA通过SIRT1/FOXO1信号轴促进胃癌细胞的自噬

VacA of H.pylori Promotes Autophagy through SIRT1/FOXO1 Signaling Axis in Gastric Cancer Cells

纯化幽门螺杆菌空泡毒素A(VacA)蛋白后与人体胃癌细胞(SGC7901)共培养,蛋白质印迹法检测SGC7901细胞中沉默调节蛋白1(SIRT1)、叉头框蛋白O(FOXO)1及自噬相关蛋白(P62)的表达情况,并通过RNA干扰(siRNA)技术沉默SIRT1的表达,研究SIRT1/FOXO1信号轴与自噬的相互关系.研究结果显示,VacA蛋白处理胃癌细胞后,SIRT1及FOXO1蛋白表达水平升高,P62蛋白表达水平降低,SGC7901细胞自噬增强.通过干扰SIRT1表达,能够降低FOXO1蛋白表达,增强P62的表达,VacA蛋白诱导的SGC7901细胞自噬受到抑制.提示幽门螺杆菌VacA能够通过调节SIRT1/FOXO1信号轴促进胃癌细胞的自噬.

Human gastric cancer cell SGC7901 was treated with VacA protein purified from H.pylori.The expressions of SIRT1,FOXO1 and P62 in SGC7901 cells were detected by Western blot.Then the expression of SIRT1 was silenced by siRNA technology,and the correlation between SIRT1/FOXO1 signal axis and autophagy was determined.The results showed that VacA increased the expression levels of SIRT1 and FOXO1,decreased the expression levels of P62,and enhanced autophagy in SGC7901 cells.By interfering with SIRT1 expression,FOXO1 protein expression was decreased and P62 expression was enhanced.VacA protein induced autophagy in SGC7901 cells was inhibited.These results suggested that VacA can promote autophagy in gastric cancer cells by regulating the SIRT1/FOXO1 signal axis.