p63与UNC5D在冬凌草甲素诱导的膀胱癌细胞凋亡中的表达

摘要

Objective To investigate the expression of p63 and UNC5 family during apoptosis induced by oridonin in 5637 cells with mutant p53. Methods Cell survival after oridonin treatment was detected with MTT assay,cell apoptosis was examined by TUNEL assay and expression of pro-apoptotic genes was analyzed by RT-PCR and Western blot. Results 5,10,20 μmol/L oridonin could differently inhibit the survival and induce apoptosis of 5637 cells in a dose-dependent manner. Oridonin significantly induced the co-expression of p63 and UNC5D, whereas the expression of p53, UNC5A-C and netrin-1 were unchanged. Conclusion Oridonin could induce apoptosis in p53 mutant bladder cancer cells with a dose-dependent manner. The possible mechanism might be due to up-regulation of p63 and UNC5D expression.%目的 探讨p63与UNCSD在冬凌草甲素(oridonin)诱导的p53突变型膀胱癌细胞系5637凋亡过程中的表达.方法应用MIT比色法检测oridonin对5637细胞存活的影响,TUNEL法检测细胞凋亡,RT-PCR检测凋亡相关基因mRNA表达,Western blot法检测p63、UNC5D蛋白表达.结果 浓度为5,10,20 μmol/L的oridonin以剂量依赖方式有效抑制5637细胞的存活并诱导凋亡(P＜0.05).oridonin处理可明显诱导p63和UNC5D的共同表达,而p53及UNC5家族其他成员的表达无明显变化.结论 oridonin能以剂量依赖的方式有效诱导p53突变型膀胱癌细胞5637的凋亡,其作用机制可能与上调促凋亡基因p63、UNC5D的表达有关.