肿瘤坏死因子-α促进乳腺癌细胞MCF-7迁徙的机制探讨  

The mechanism of tumor necrosis factor-α promoting migration in breast cancer cell line MCF-7

作　　者：殷咏梅[1] 李俊[1] 李晓东[1] 梗一婷[1] 束永前[1] 

机构地区：[1]南京医科大学第一附属医院肿瘤科,南京210029

出　　处：《临床肿瘤学杂志》2009年第12期1064-1068,共5页Chinese Clinical Oncology

基　　金：国家自然科学基金资助项目(NO.30772474);江苏省自然科学基金(BK2008477);江苏省卫生厅开放课题(XK18200904)

摘　　要：目的:探讨肿瘤坏死因子(tumor necrosis factor-α,TNF-α)诱导黏附分子CD44表达的机制。方法:以0、2、20、200ng/ml浓度处理MCF-7细胞,了解对MCF-7细胞增殖以及迁徙的影响。Western-blot方法检测MAPK(JNK、P38、ERK)信号通路中蛋白磷酸化水平的变化;用MAPK抑制剂预处理后,检测CD44表达水平。结果:TNF-α可以改变CD44亚型表达,并促进MCF-7细胞的迁徙能力;TNF-α可以激活JNK信号转导通路,对P38和ERK信号通路无明显激活效应;用特异性的JNK信号通路抑制剂可以阻断TNF-α诱导的CD44蛋白表达水平。结论:TNF-α通过JNK信号通路调节CD44并促进MCF-7细胞的迁徙能力。Objective：To investigate the mechanism of tumor necrosis factor-or promoting migration via CD44 expression in MCF-7 ceils. Methods：To treat MCF-7 with different concentration of TNF-α（0,2,20,200ng/ml） and detect the proliferation and migration ability. Using Western blot to detect the expression of CIM4 protein and the phosphorylation status of p-JNK, p-P38 and p- ERK. Results：TNF-α promoted migration ability of MCF-7 via differentially modulates the expression of CD44. TNF-α could up-regulate expression of CD44 by the activation of JNK, which was reversed by pre-treatment with JNK-inhibitor SP600125, P38 and ERK pathway seemed not involved in TNF-α induced MCF-7 migration. Conclusion：These data suggest that the pro-inflammatory cytokine TNF-α differentially modulates CD44 expression and promotes migration ability in MCF-7, via a JNK pathway.

关 键 词：肿瘤坏死因子-Α 迁徙 细胞黏附分子 CD44 JNK P38 ERK 

分 类 号：R737.9[医药卫生—肿瘤]