甲基化EGCG对SGC 7901细胞Cyclin E、Bcl-2、Bcl-xL表达影响与抑癌作用研究

目的：观察甲基化表没食子儿茶素没食子酸酯（methylated epigallocatechin gallate,甲基化EGCG）对胃癌SGC 7901细胞Cyclin E、Bcl-2、Bcl-xL表达的影响,探讨甲基化EGCG抗肿瘤的作用机制。方法：采用MTT法观察甲基化EGCG对胃癌细胞SGC 7901增殖的影响,采用免疫细胞化学方法、Western blot法分别检测Cyclin E、Bcl-2、Bcl-xL的表达。结果：甲基化EGCG呈时间依赖性抑制胃癌SGC 7901细胞增殖（P〈0.05）,下调Cyclin E、Bcl-2、Bcl-xL的表达。结论：甲基化EGCG可能通过下调Cyclin E、Bcl-2、Bcl-xL的表达,使胃癌SGC 7901细胞的增殖和凋亡之间达到平衡,从而发挥抗肿瘤作用。

Effects of methylated EGCG on the cells proliferation and expressions of Cyclin E,Bcl-2 and Bcl-xL in human gastric cancer cell line SGC 7901

Objective：To establish human gastric cancer cell line SGC 7901 as a subject and investigate the effects of methylated EGCG on the cells proliferation in vitro.To detect the expressions of the regulation proteins of cell cycle Cyclin E and anti-apoptosis protein Bcl-2 and Bcl-xL in human gastric cancer cell line SGC 7901.To explore the probably mechanism of the anti-tumor activity of methylated EGCG.Methods：The cell growth of human gastric cancer cell line SGC 7901 was quantified by MTT assay.The expressions of the regulation proteins of cell cycle such as Cyclin E and anti-apoptosis protein Bcl-2 and Bcl-xL in human gastric cancer cell line SGC 7901 were detected by immunocytochemical stainning and Western blot.Results：Human gastric cancer cell line SGC 7901 was treated with methylated EGCG after 24 h,48 h,and 72 h respectivly,the medicine inhibited the cells proliferation in a time-dependent fashion.The longer time was,the lower OD was.To compare with control,the inhibition of cell proliferation increased.Methylated EGCG could down-regulate the expressions of the regulation proteins of cell cycle Cyclin E and it also could cause the down-regulation of the expressions of anti-apoptosis protein Bcl-2 and Bcl-xL.Conclusion：Methylated EGCG may inhabit the proliferation of human gastric cancer cells SGC 7901 obviously.The underlying molecular mechanism is that methylated EGCG through down-regulating the expressions of the regulation proteins of cell cycle Cyclin E and the expressions of anti-apoptosis protein Bcl-2 and Bcl-xL result of cell cycle arrested and apoptosis induced to inhibit the cell proliferation.