泰素帝体外诱导肿瘤细胞凋亡的实验研究  

Mechanism of docetaxel-induced apoptosis in cancer cells

作　　者：李瑛[1] 石廷章[1] 焦顺昌[1] 杨俊兰[1] 魏秀芳[1] 

机构地区：[1]解放军总医院肿瘤科,北京100853

出　　处：《军医进修学院学报》2006年第2期98-99,共2页Academic Journal of Pla Postgraduate Medical School

摘　　要：目的:泰素帝体外诱导人肿瘤细胞凋亡及其机制的研究。方法:应用形态学方法、流式细胞术、DNA凝胶电泳、Annexin V标记等方法检测细胞凋亡的发生,应用RT-PCR检测凋亡相关基因Fas、bc l-2、c-myc表达的变化。结果:泰素帝可诱导人肺腺癌细胞系A549和人早幼粒性白细胞株HL60发生凋亡,凋亡率分别为15.69%和33.46%;凋亡相关基因Fas转录水平比用药前增强,bc l-2和c-myc无明显变化。结论:凋亡为泰素帝抑瘤的机制之一。泰素帝诱导肿瘤凋亡可能主要与促进Fas基因表达有关。Objective：To study the anti-tumor effect of docetaxel and investigate induction of apoptosis and its mechanism. Methods：Morphological study, DNA gel electrophoresis, flow cytometry and fluorescein labelled Annexin V to detect apoptosis,RT-PCR to detect the gene related with apoptosis. Results：docetaxol can induce apoptosis in A549 cells and Hlf30 cells. The proportion of apoptosis is 15.69% and 33.46%. Fas gene was enhanced. Conclusion：docetaxel induced apoptosis and necrosis of human tumor cells is the key mechanism for its killing action in the treatment of cancer.

关 键 词：泰素帝 细胞凋亡 基因 BCL-2 

分 类 号：R730.5[医药卫生—肿瘤]