p63与UNC5D在冬凌草甲素诱导的膀胱癌细胞凋亡中的表达

 目的探讨p63与UNC5D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MTT 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与UNC5D及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与UNC5D的表达有关。

Expression of p63 and UNC5D during Oridonin-Induced Apoptosis in Bladder Cancer Cell Line

Objective To investigate the expression of and family during apoptosis induced by oridonin in 5637 cells with mu-tant . 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 p63of and LNC5D，whereas the expression of p53 ，UNC5A-C and netrin-l  were unchanged. Conclusion Oridonin could induce apoptosis in p53 mu-tant bladder cancer cells with a dose-dependent manner. The possible mechanism might be due to up-regulation of p63 UNC5D and expres-sion.