非小细胞肺癌中Twist通过TGF-β／Smad3信号通路促进EMT的发生

摘要

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（EM T ）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EM T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，E-cadherin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EM T 的发生。%Objective:To investigate the role of Twist which may induce EMT through TGF-β/Smad3 pathway in NSCLC ,the expression of Twist ,Smad3 ,E-cadherin and Vimentin molecules were detected and the cor-relations were discussed .Methods :Twist ,Smad3 ,E-cadherin and Vimentin expressions in tumor tissues were as-sessed using immunohistochemical (IHC) methods in patients with resected NSCLC ,and the correlation of Twist with Smad3 ,Smad3 with E-cadherin and Vimentin expression were analyzed .Results :The expression of Twist、Smad3、Vimentin were mainly located in cytoplasm and cell nucleus ,and the expression of E-cadherin was mainly lo-cated on cell membrane .The positive expression rates of Twist ,Smad3 ,E-cadherin and Vimentin protein in NSCLC were 72 .3% (120/166) ,71 .1% (118/166) ,54 .2% (90/166) ,69 .9% (116/166) ,which were higher than corre-sponding adjacent non-cancerous tissue with statistical difference ( P< 0 .001 ) . The correlation of Twist with Smad3 ,Smad3 with E-cadherin and Vimentin were obvious in pathological grads and TNM stages groups in NSCLC .Conclusion:Twist may induce EMT in NSCLC by regulating the TGF-β/Smad3 signaling pathway .