紫杉醇诱导MCF-7凋亡与bcl-2及bax的关系

Paclitaxel-induced apoptosis corelated with down-regulation of Bcl-2 and up-regulation of bax in MCF-7 breast cancer cell

目的 探讨抗肿瘤药物紫杉醇及顺铂诱导肿瘤细胞凋亡机制。方法 用紫杉醇及顺铂诱导乳腺癌细胞系MCF 7凋亡 ,采用TUNEL、电镜及免疫组化SP法分别检测凋亡及与凋亡相关基因bcl 2、Bax表达的动态变化。结果 ①顺铂仅导致乳腺癌细胞系MCF 7坏死 ,不能诱导其凋亡 ;②紫杉醇可诱导MCF 7细胞凋亡并具有时间及剂量依赖性 ;③bcl 2降低、bax增加具有时间及剂量依赖性。结论 紫杉醇诱导MCF 7细胞凋亡与bcl 2降低及bax增加有关。

AIM To investigate the effect of paclitaxel and cisplatin on apoptosis of MCF 7 and its mechanism. METHODS The apoptotic cells were detected by TUNEL method and the expression of Bcl 2 and bax were examined using immunohistochemistry S P method in different time. RESULTS Cisplatin resulted in the death of MCF 7, but did not cause the apoptois of MCF 7. Paclitaxel caused time dependent and concentration dependent increases in the apoptotic cells. Treatment of MCF 7 cells with paclitaxel resulted in time and concentration dependent decreases in bcl 2 and increased in bax proteins. CONCLUSION The apoptosis induced by paclitaxel is related to the increase of bax protein and the decrease of bcl 2 protein.