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目的研究转化生长因子β1(TGF-β1)诱导的跨膜蛋白(TMEPAI)在乳腺癌的进展过程中所起作用及其机制。方法采用Western blot法检测“三阴性”乳腺癌、正常乳腺组织及不同乳腺癌细胞系中TMEPAI蛋白水平。TGF-β1和TGF-β1受体I激酶(Alk5)抑制剂SB431542处理M DA-M B-231和Hs 578Bst细胞,检测内源性TM E-PAI的水平。Smad7、Alk5和显性抑制TGF-β11受体I(DN Alk5)质粒转染细胞,检测TM EPAI表达水平的变化。敲低MDA-MB-231细胞中的TMEPAI,检测细胞中人第10号染色体缺失的磷酸酶及张力蛋白同源的基因(PTEN)和p27Kip1的表达变化。结果 “三阴性”乳腺癌组织和细胞系中存在TMEPAI过表达,而正常组织和M CF-7细胞系中无TM EPAI表达,差异具有统计学意义(P<0.05)。结论乳腺癌细胞TGF-β1通路激活导致TM EPAI过度表达,TM EPAI通过影响多种肿瘤相关蛋白表达促进乳腺癌发展。
Objective To investigate the role and mechanism of TMEPAI induced by transforming growth factor-β1 (TGF-β1) in the progression of breast cancer. Methods Western blot was used to detect TMEPAI protein levels in “triple negative” breast cancer, normal breast tissue and different breast cancer cell lines. M DA-M B-231 and Hs 578 Bst cells were treated with TGF-β1 and TGF-β1 Receptor I Kinase (Alk5) inhibitor SB431542 to detect the level of endogenous TM E-PAI. Smad7, Alk5 and dominant-negative TGF-β11 receptor I (DN Alk5) plasmids were transfected into the cells to detect the changes of TM EPAI expression. TMEPAI in MDA-MB-231 cells was knocked down and the expression of PTEN and p27Kip1, which are human chromosome 10-deficient phosphatase and tensin homology genes, was detected in the cells. Results There was TMEPAI overexpression in the “triple negative” breast cancer tissues and cell lines, but there was no TM EPAI expression in the normal tissues and the M CF-7 cell lines. The difference was statistically significant (P <0.05). Conclusion The activation of TGF-β1 pathway in breast cancer cells leads to the overexpression of TM EPAI. TM EPAI promotes the development of breast cancer by affecting the expression of various tumor-associated proteins.