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机构地区:[1]中国医科大学附属第一医院干诊科,辽宁沈阳110001 [2]中国医科大学附属第一医院骨外科,辽宁沈阳110001
出 处:《现代肿瘤医学》2009年第8期1407-1410,共4页Journal of Modern Oncology
基 金:国家自然科学基金科学部主任基金资助项目(编号:30640001)
摘 要:目的:探讨细胞周期蛋白酶抑制剂flavopiridol(FP)对耐阿霉素尤文肉瘤细胞增殖抑制及凋亡诱导的作用机制。方法:采用MTT法测定阿霉素(ADM)及falvopiridol对VH-64/ADR细胞的半数抑制浓度(IC50),计算耐药倍数;流式细胞计数仪(FCM)检测falvopiridol给药后VH-64/ADR细胞周期的变化;West-ern-blotting方法检测细胞中Bcl-2、pro-caspase-3、活化型多聚ADP核糖多聚酶(PARP-85)蛋白的表达。结果:flavopiridol可抑制尤文肉瘤耐阿霉素细胞株VH/ADR的细胞增殖,其效果呈时间及浓度相关性(P<0.05)。flavopiridol给药后,耐药细胞株VH-64/ADR的细胞凋亡率明显高于对照组(P<0.05);bcl-2、pro-casepase-3表达下调,而活性型PARP表达上调。结论:FP可有效诱导VH-64/ADR细胞发生凋亡,其机制可能与线粒体信号传导途径有关。Objective: To investigate the growth - inhibitory and apoptosis inducing effect of flavopiridol on human Ewing Sarcoma VH - 6d/ADR cell and its mechanism in vitro. Methods : The proliferation of VH - 64 and VH - 64/ ADR cells was determined by using MTT method. Cell cycle progression and apoptosis ratio were determined by flow cytometry. The expression of bcl - 2, cleaved - PARP, casepase - 3 were detected by western blot. Results: After exposure to flavopiridol, the growth of VH - 64/ADR cells were inhibited in a both time - dependent and dose - dependent manner(P 〈 0.05). Apoptosis rate of VH - 64/ADR was higher than that of control group ( P 〈 0.05 ). The expression of bcl - 2 and pro - casepase - 3 were down - regulated, and the expression of active - form PARP was up - regulated. Conclusion: The apoptosis of VH - 64/ADR cells induced by flavopiridol might be via mitochondrial pathway.
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