紫杉醇诱导乳腺癌细胞凋亡的分子生物学机制  

Molecular biological mechanism of paclitaxel induced apoptosis in breast cancer cells

作　　者：柳光宇[1] 邵志敏[1] 沈镇宙[1] 

机构地区：[1]上海医科大学附属肿瘤医院外科,上海200032

出　　处：《中国癌症杂志》2000年第1期93-96,共4页China Oncology

摘　　要：紫杉醇具有促微管聚合及使细胞分裂停滞的作用 ,但这一作用并非导致人类乳腺癌细胞凋亡的直接原因。近年来的分子生物学研究提示紫杉醇可能通过启动了与细胞凋亡相关的信号传导通路及一系列蛋白质修饰过程而发挥细胞毒性作用。其中抗凋亡蛋白bcl 2的磷酸化似乎起关键性作用 ,在其上游包括c Raf 1和PKA ,下游还有caspase 3、PARP等都可能参与这一诱导凋亡过程。此外p34cdc 2激酶、p35和p2Paclitaxel(taxol)can promote the polymerization of micotubules and block the mitosis, but it is not the direct mechanism of aopotosis of human breast cancer cells.Recent moecular biological researches suggest that there could be an apoptosis concerned signal transduction pathway and a series of proteins modified courses which induced by taxol and cause the cellular toxicity. The phosphorylation of anti apoptotic protein bcl 2 may be the key of the procedure,and other involved proteins include c Raf 1,PKA upstream and caspase 3,PARP downstream. In volvement of p34cd 2 kinase,p53 and p21 have also been reported.

关 键 词：紫杉醇 乳腺癌 细胞凋亡 分子生物学 

分 类 号：R737.9[医药卫生—肿瘤] R979.1[医药卫生—临床医学]