Rab25 siRNA诱导人卵巢癌细胞凋亡及其机制的研究  

The mechanism of Rab25 small interfering RNA inducing ovarian cancer cells apoptosis

作　　者：樊杨[1] 辛晓燕[1] 陈必良[1] 马向东[1] 商莉[2] 

机构地区：[1]第四军医大学西京医院妇产科,西安710032 [2]宁夏回族自治区人民医院妇产科

出　　处：《现代妇产科进展》2008年第1期23-26,共4页Progress in Obstetrics and Gynecology

摘　　要：目的:通过RNA干涉抑制Rab25在人卵巢上皮性癌的过表达,探讨Rab25siRNA对肿瘤细胞凋亡的生物学效应及作用机制。方法:构建针对Rab25的siRNA重组质粒,稳定转染A2780细胞,通过RT-PCR检测Rab25的表达,用Hoechst 33258染色和TUNEL法研究Rab25 siRNA诱导细胞的凋亡;用免疫组化法分析抑制Rab25的表达对凋亡相关蛋白Bcl-2和Bax表达的影响。结果:Rab25 siRNA可诱导肿瘤细胞凋亡;蛋白水平检测表明抑制Rab25表达使Bcl-2表达下降,Bax表达增强。结论:Rab25 siRNA可诱导细胞凋亡,Rab25影响卵巢癌细胞生存途径是通过调节Bcl-2/Bax表达含量发挥作用。Objective：To investigate the biological effect of siRNA of Rab25 on human carcinoma cell and its mechanism. Methods：According to Rab25 mRNA sequence in the Gene-bank, the plasmids expressing siRNA against Rab25 were constructed and stably transected into 322780 cells;Rab25 expression was detected by RT-PCR. Hoechest 33258 staining and TUNEL were used to determine apoptosis. Immunohistochemistery was performed to analysis apoptofic proteins expression. Results： Rab25 siRNA in ovarian carcinoma cells could induce apoptosis and down-regulate the expression of anti-apoptotic protein Bcl-2 and increase the expression of Bax. Conclusion： Rab25 siRNA induces ovarian carcinoma cell apoptosis via down-regulation of Bcl-2 and up-regulation of Bax.

关 键 词：卵巢肿瘤 RAB25 小干扰RNA 细胞凋亡 基因BCL-2 基因BAX 

分 类 号：R737.31[医药卫生—肿瘤]