多西紫杉醇诱导人乳腺癌MCF-7细胞凋亡及相关基因表达的影响

目的探讨多西紫杉醇(docetaxcel)诱导体外培养人乳腺癌MCF-7细胞凋亡的作用及凋亡的分子机制。方法通过MTT比色法分析多西紫杉醇对人乳腺癌MCF-7细胞增殖的影响;应用光镜、电镜观察细胞形态学的改变;Annexin-V/PI双染流式细胞术检测肿瘤细胞周期动力学和凋亡诱导率的影响;免疫组化方法检测凋亡相关基因bax、bc1-2的表达变化。结果多西紫杉醇可明显抑制人乳腺癌MCF-7细胞的增殖,并可导致其形态学的改变;随着加药时间的增长,G2/M期细胞增多,G2/M期细胞和S期细胞的比值也随剂量呈递增关系;加药(IC50)48h后早期凋亡细胞明显增多,同时可上调bax和下调bc1-2的蛋白表达量。结论多西紫杉醇可明显抑制MCF-7肿瘤细胞的生长,诱导细胞凋亡。其分子机制可能与激活bax和抑制bc1-2等凋亡调控基因有关。

Docetaxcel Induces Apoptosis and Regulates Expressions of bax and bcl-2 Protein in Human Breast Carcinoma MCF-7 Cells

Objective To study the inducing apoptosis of docetaxcel on MCF-7 cell and the might molecular mechanism. Methods Inhibition of MCF-7 cell proliferation was measured,using MTT assay. The morphological alterations were confirmed by microscopy though double staining.The amount of apoptosis cell and the changes of cell cycle were measured by flow cytometry after the otlls were stained with Annexin-V and PI. The expression of apoptosis associated gene was analyzed by immune assembly chemistry. Results Docetaxcel has significant inhibition on the growth of MCF-7. The marked morphologica changed and the increased apoptosis cells were observed. Moreover, docetaxcel G2/M phrase cells. The expression of the gene bax raised and bcl-2 decreased. Conclusion Docetaxcel is able to lead tumor cells apoptosis, the activation of bax and the suppression of bcl-2 may contribute to the apoptosis mechanism.