HSP 90与survivin在人乳腺癌细胞中的作用及机制探讨  

The interaction between HSP 90 and survivin in human breast cancer cells and its underlying mechanism

作　　者：余畅[1] 邓华瑜[1] 

机构地区：[1]重庆医科大学病理生理教研室,重庆400016

出　　处：《肿瘤》2007年第10期791-794,共4页Tumor

基　　金：重庆市科技计划项目(编号:CSTC;2005AC0075)

摘　　要：目的:研究热激蛋白90(heat shock protein 90,HSP 90)和survivin在人乳腺癌细胞中的相互作用以及对肿瘤细胞增殖、凋亡的影响。方法:以人乳腺癌细胞MDA-MB-231为研究对象,用HSP 90抑制剂格尔德霉素(geldanamycin,GA)处理后,Western印迹法检测细胞中P-STAT3、survivin蛋白表达的变化;RT-PCR检测survivin mRNA的变化;MTT法检测其对细胞的增殖活性影响;流式细胞术检测凋亡的变化。结果:HSP90抑制剂GA可使人乳腺癌细胞MDA-MB-231中P-STAT3减少、survivin的蛋白表达减少,细胞的增殖活性降低,凋亡增多。结论:在MDA-MB-231细胞中,HSP 90可能通过激活JAK-STAT3信号通路,影响survivin转录表达,共同促进该肿瘤细胞的高增殖、低凋亡的恶性行为。Objective：To study the interaction between heat shock protein 90 （HSP90） and the survivin in human breast cancer cells and its effect on proliferation and apoptosis of tumor cells. Methods： The human breast cancer MDA-MB-231 cells were treated with an HSP90 inhibitor, geldanamycin （GA）. The expression of phosphorylated signal transducers and activators of transcription 3 （P-STAT3） and survivin protein were detected by Western blotting. The mRNA transcription of sruvivin was determined by RToPCR. The cell proliferation was measured by MTr assay. Apoptosis was examined by flow cytometry. Results： HSP 90 inhibitor GA reduced the expression of P-STAT3 and survivin, inhibited the proliferation, and induced apoptosis of human breast cancer MDA-MB-231 cells. Conclusion： HSP90 affected the transcription of survivin mRNA through activation of the JAK-STAT3 signaling pathway. Survivin- HSP90 interaction contributed to the promotion of the high-proliferation and low-apoptosis malignant behaviors of human breast cancer MDA-MB-231 cells.

关 键 词：乳腺肿瘤 热休克蛋白质类90 信号转导 SURVIVIN 格尔德霉素 MDA-MB-231细胞 

分 类 号：R737.9[医药卫生—肿瘤]