摘要
目的 探讨泰素帝诱导人肺腺癌细胞凋亡的作用机制。方法 应用形态学方法、流式细胞术 (FACS)、DNA凝胶电泳、AnnexinV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、bcl 2、c myc表达的变化。结果 泰素帝对人肺腺癌细胞系A5 49细胞的生长有明显的抑制作用 ,使细胞分裂阻滞于G2M期 ,并诱导肿瘤细胞发生凋亡。凋亡细胞表现为细胞固缩 ,核染色质聚集或断裂 ,DNA凝胶电泳显示清晰的DNA梯形条带 ,FAGS检测在G1期之前出现sub G1峰 ,凋亡率最高为 15 6 9% ,AnnexinV标记的方法检测凋亡时发现 ,坏死和凋亡共存。在泰素帝诱导A5 49凋亡的过程中 ,凋亡相关基因Fas转录水平比用药前增强 ,bcl 2和c myc无明显变化。结论 除了坏死 ,凋亡也为泰素帝抑瘤的机制之一。泰素帝诱导A5
Objective To study the mechanism of docetaxel induced apoptosis. Methods Morphological study, DNA gel electrophoresis, flow cytometry and fluorescin labeled Annexin V to detect apoptosis, RT PCR to detect the gene related with apoptosis. Results Human lung cancer A549 cells treated with docetaxel induced cell cycle arrest at G 2M phase, leading to apoptosis. The morphology of A549 cells showed nuclear chromatine condensation and fragmentation. Typical ladder pattern of DNA fragmentation was observed. Sub G 1 peak was found by flow cytometry. Transcription of Fas gene was enhanced, while no change in c myc and bcl 2 genes. Annexin labeling results revealed the co existense of cell apoptosis and necrosis in docetaxel treated A549 cells. Conclusion Docetaxel induces apoptosis and necrosis of human lung cancer. The induction of apoptosis may be related to expression of Fas.
出处
《中华肿瘤杂志》
CAS
CSCD
北大核心
2000年第3期208-211,共4页
Chinese Journal of Oncology
