幽门螺杆菌诱导胃癌细胞凋亡与p53状态和bax、caspase表达的关系

Relation of apoptosis induced by helicobacter pylori in gastric cancer cells with p53 protein status and expression of bax and caspase

目的探讨幽门螺杆菌（HP）体外诱导胃癌细胞凋亡与p53状态和bax、caspase表达的关系。方法流式细胞术检测HP国际标准菌株NCTC11637诱导SGC-7901和AGS细胞凋亡，检测NCTC11637对SGC-7901和AGS的bax、caspasemRNA和蛋白表达的影响。结果HP能够在体外直接诱导SGC-7901和AGS细胞凋亡，SGC-7901细胞发生凋亡的高峰时间出现在12～24h，AGS细胞的凋亡率则随着HP感染时间的延长而增高。HP能够呈时间依赖性地上调SGC-7901和AGS细胞的BaxmRNA和蛋白表达，并促进caspase-9和caspase-3的激活。结论幽门螺杆菌可以通过线粒体途径直接诱导胃癌细胞凋亡，而且野生型p53具有放大线粒体凋亡途径的作用。

Objective To investigate the apoptosis of gastric cancer cells induced by Helicobacter（HP） in vitro and the relationship with p53 protein status and expression of bax and caspase. Methods Apoptosis was evaluated in human adenocarcinoma cell lines SGC-7901 and AGS cells by flow cytometry and expression of bax and caspase was examined. Results NCTC 11637 induced apoptosis in SGC-7901 and AGS cells in vitro. The peak of apoptosis index occurred beween 12-24h in SGC-7901 after NCTC 11637 infection and the apoptosis index of AGS increased along with the time of NCTC 11637 infection. NCTC 11637 could upregulate bax mRNA and protein expression in SGC-7901 and AGS cells and induced a time dependent activation of caspase-9 and -3. Conclusion HP may directly induce gastric cancer cells apoptosis through mitochondrial apoptotic pathway and wild-type p53 amplifies this process.