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目的:探讨非小细胞肺癌(NSCLC)组织转录因子Twist调控TGF-β/Smad3的表达,促进上皮间质转化(EMT)的发生机制。方法:采用免疫组织化学法检测NSCLC组织样本中Twist、TGF-β/Smad3以及EMT中代表性分子E-cadherin和Vimentin蛋白表达,并统计分析二者表达之间的相关性。结果:Twist、Smad3、Vimentin蛋白阳性着色定位于细胞质和细胞核内,Ecadherin蛋白阳性着色定位于细胞膜。Twist、Smad3、E-cadherin、Vimentin蛋白在NSCLC中阳性率分别为72.3%(120/166)、71.1%(118/166)、54.2%(90/166)、69.9%(116/166),显著高于癌旁组织,差异有统计学意义。Twist与Smad3、Smad3与E-cadherin、Vimentin在NSCLC不同分化程度及不同TNM分期均呈显著相关。结论:NSCLC中Twist可能通过TGF-β/Smad3信号通路促进EMT的发生。
Objective: To investigate the mechanism of Twist regulating the expression of TGF-β / Smad3 and promoting epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC). Methods: The expression of Twist, TGF-β / Smad3 and E-cadherin and Vimentin protein in NSCLC tissues were detected by immunohistochemistry. The correlation between them was statistically analyzed. Results: Positive staining of Twist, Smad3 and Vimentin localized in the cytoplasm and nucleus, and positive staining of Ecadherin protein localized in the cell membrane. The positive rates of Twist, Smad3, E-cadherin and Vimentin in NSCLC were 72.3% (120/166), 71.1% (118/166), 54.2% (90/166) and 69.9% (116/166) Higher than the paracancerous tissue, the difference was statistically significant. Twist and Smad3, Smad3 and E-cadherin, Vimentin in NSCLC different degrees of differentiation and different TNM staging were significantly related. Conclusion: Twist may promote EMT via TGF-β / Smad3 signaling pathway in NSCLC.