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目的:观察幽门螺杆菌(H.pylori,HP)作用于食管癌细胞(ECa-109)后细胞凋亡的情况以及细胞色素氧化酶Ⅱ(cytochrome oxidaseⅡ,COXⅡ)、Bax、Caspase-3 mRNA及其蛋白表达的变化,探讨H.pylori致癌的分子机制。方法:将H.pylori与ECa-109分别作用4、8、24 h,收集各组细胞,流式细胞术(FACS)检测凋亡情况;Real-Time PCR和Western blot法检测各时间点COXⅡ、Bax、Caspase-3 mRNA及其蛋白表达。结果:随着共培养时间的延长,COXⅡmRNA和蛋白的表达逐渐下降,而Bax、Caspase-3 mRNA和蛋白的表达逐渐上升,ECa-109凋亡增加。结论:H.pylori可抑制食管癌细胞线粒体编码基因COXⅡmRNA的表达,从而影响线粒体功能;H.pylori在体外可通过线粒体途径上调Bax、Caspase-3表达,从而诱导ECa-109凋亡。
Objective: To observe the apoptosis of human esophageal cancer cells (ECa-109) induced by Helicobacter pylori (H.pylori) and the expression of cytochrome oxidaseⅡ (COXⅡ), Bax and Caspase-3 mRNA Protein changes, to explore the molecular mechanism of H.pylori carcinogenesis. Methods: The cells were collected for 4, 8 and 24 hours respectively after treated with H.pylori and ECa-109. The apoptosis of the cells was detected by flow cytometry (FCM). The expression of COXⅡ, Bax, Caspase-3 mRNA and protein expression. Results: With the extension of co-culture time, the expression of COXⅡmRNA and protein decreased gradually, while the expression of Bax, Caspase-3 mRNA and protein gradually increased, and the apoptosis of ECa-109 increased. Conclusions: H.pylori can inhibit the expression of mitochondrial COX Ⅱ mRNA in esophageal cancer cells and thus affect the function of mitochondria. In vitro, H.pylori can up-regulate the expression of Bax and Caspase-3 through mitochondrial pathway to induce the apoptosis of ECa-109.