HP培养滤液诱导下抑制bcl-2基因表达对SGC7901细胞端粒酶活性的影响

目的:探讨bcl-2表达与hTERT、端粒酶活性之间的调控关系,了解HP的致癌机制。方法:在HP培养滤液诱导前后,采用流式细胞仪检测bcl-2AODN抑制bcl-2基因之后人SGC7901细胞hTERT蛋白的表达。结果:对照组人SGC7901细胞24h、36h和48h表达hTERT蛋白的阳性细胞数和荧光指数显著低于经HP培养滤液诱导的SGC7901胃癌细胞组(P<0.05)。在HP滤液诱导下,抑制bcl-2基因的SGC7901胃癌细胞24h、36h和48h表达hTERT蛋白的阳性细胞数和荧光指数显著低于与SGC7901胃癌细胞(P<0.05),同时显著高于对照组(P<0.05)。结论:bcl-2基因正向调控hTERT蛋白表达,bcl-2表达上调可能是端粒酶活化的主要途径之一。端粒酶的激活不完全依赖于bcl-2途径,还存在其他的调控因素。HP感染不仅通过上调bcl-2的表达,还可以通过其他途径激活端粒酶,这可能是HP感染致癌的一条重要途径。

Effects of H. pylori incubation filtrate on expression of bcl-2 protein in human 7901 gastric carcinoma cells transferred antisense hTERT

Objective:To explore the relationship between the expression of bcl-2 protein and hTERT and activity of telomerase, and to study the carcinogenic mechanism of H. pylori.Methods:The hTERT protein expressions in SGC7901 cells transferred antisense bcl-2 gene were detected by flow cytometry(FCM) before and after incubated with low concentration of H. pylori incubation filtrate. Results:The number of cells expressing hTERT protein and the fluorescent index of hTERT protein in the control SGC7901 cells were significantly lower than those in the SGC7901 cells cultured with H. pylori incubation filtrate at 24, 36 and 48 h(P<0.05). Under induction of H. pylori incubation filtrate, the number of the positive cell and the fluorescent index of hTERT protein in SGC7901 cells where the expression of bcl-2 gene was inhibited were significantly lower those in the SGC7901 cells cultured with H. pylori incubation filtrate and higher than those in the control SGC7901 cells t 24, 36 and 48 h(P<0.05).Conclusion:Bcl-2 gene could up-regulate the expression of hTERT protein. The up-regulation of bcl-2 expression may be one of the main mechanisms of activation of telomerase. The activation of telomerase was induced not only by the up-regulation of bcl-2 expression, but also by other factors. H. pylori infection activates telomerase not only through up-regulating expression of bcl-2, but also through other approaches, which might be one of the carcinogenic mechanisms of H. pylori.