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作 者:王薇[1] 柯舜安[2] 邬素芳 李静[1] 陈刚[1] 李辅军 王世宣[1] 卢运萍[1] 马丁[1]
机构地区:[1]华中科技大学同济医学院附属同济医院,湖北武汉430030 [2]三峡大学第一临床医学院,湖北宜昌443000
出 处:《实用妇产科杂志》2005年第5期276-278,i001,共4页Journal of Practical Obstetrics and Gynecology
基 金:国家重点基础研究发展项目(2002CB513100)
摘 要:目的探讨拓扑替康(TPT)诱导人卵巢癌顺铂耐药株COC1/DDP凋亡的内在分子机制。方法采用透射电镜和TUNEL法观察TPT诱导COC1/DDP细胞凋亡的情况;采用RTPCR和Westernblot检测TPT对COC1/DDP细胞内bcl2、bax和caspase3基因表达的影响以及caspase3活性的改变。结果COC1/DDP细胞在TPT作用后出现典型的凋亡形态特征,且凋亡率由8.54%上升为19.31%(P<0.05);TPT不影响COC1/DDP细胞内bcl2mRNA表达,却明显增加baxmRNA和caspase3mRNA表达,并提高caspase3活性。结论TPT诱导COC1/DDP细胞凋亡可能依赖于细胞内bax蛋白增高和caspase3的活化。Objective:To explore the molecular mechanism of topotecan-induced apoptosis in cisplatin-resistant human ovarian cancer cell line COC1/DDP. Methods:Transmission electron microscope(TEM) and TUNEL were employed to observe the apoptosis of COC1/DDP induced by topotecan. RT-PCR and Western blot were used to determine the expression of bcl-2,bax and caspase-3.Changes of the activity of caspase-3 were also recorded. Results:After incubated with topotecan, COC1/DDP cell demonstrated a typical apoptosis morphology The apoptotic rate increased from 8.54% to 19.31%(P<0.05).Although the expression of bcl-2 was not affected, the expression of bax and caspase-3 were upregulated and the caspase-3 activity was promoted in the course of COC1/DDP apoptosis when treated with topotecan. Conclusion:The increased bax expression and the promoted caspase-3 activity may play a crucial role in the apoptosis process of COC1/DDP induced by topotecan.
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