SAHA诱导的p21表达致U251MG细胞抗凋亡效应  

SAHA-induced p21 expression results in anti-apoptotic effects in U251MG cells

作　　者：龚爱华[1,2] 熊二梦[1] 张严[1] 杜凤移[1] 彭琬昕[1] 邵根宝[1] 金洁[1] 程建军[1] 

机构地区：[1]江苏大学基础医学与医学技术学院,江苏镇江212013 [2]癌基因及相关基因国家重点实验室,上海市肿瘤研究所,上海200032

出　　处：《中国药理学通报》2013年第12期1743-1747,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 31100964,8137218);江苏省高校自然科学基金资助项目(No N07KJB310018);癌基因及相关基因国家重点实验室开放课题资助项目(No 90-13-05)

摘　　要：目的探讨SAHA诱导的p21在脑胶质瘤细胞U251MG中的生物学作用。方法采用免疫印迹技术、RAN干扰技术和流式细胞技术分析了p21的表达水平与SAHA引起的U251MG细胞周期阻滞和细胞死亡的相关性。结果与对照组相比较,p21-ShRNA组明显提高了U251MG细胞凋亡的比例,达到45%左右,活化的凋亡相关蛋白Caspase-3,-8,-9表达水平明显增加;p21-ShRNA组细胞周期调控蛋白cdc25c、cdc2的磷酸化水平和总蛋白质水平也明显上调,clycinB1和磷酸化的H3水平明显提高。结论在SAHA处理条件下,p21下调使U251MG细胞阻滞于细胞周期G2/M期,促进了细胞凋亡。Aim To determine the roles of p21 in SA- HA effects on U251MG ceils. Methods Western blot and FACS were used to examine the correlations of ex- pression of p21 with cell cycle and cell apotosis in U251MG cells treated with SAHA. Results SAHA upregulated p21 expression in a time-dependent man- ner, and induced cell cycle arrest at G1 phase, p21 knockdown significantly promoted cell death compared with control group via apoptosis pathway. Furthermore,p21 knockdown resulted in increases in phosphorylation and total protein levels of cdc25c and cdc2, as well as cyclin B1 and phosphorylated H3. Conclusions SA- HA-induced p21 plays the roles in blocking cell cycle progress and anti-apoptosis, which might provide the evidence for further clinical research on SAHA against glioma cells.

关 键 词：SAHA 胶质瘤细胞 P21 凋亡 细胞周期 RNA干扰 组蛋白去乙酰化酶 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学] R329.28[医药卫生—基础医学]