TMEM206促进表皮生长因子诱导的结直肠癌上皮-间质转化

TMEM206 promotes epidermal growth factor-induced epithelial-mesenchymal transition in colorectal cancer cells

目的研究TMEM206在结直肠癌发生、发展中的作用及其机制。方法将结直肠癌细胞HCT116和SW480均随机分为4组,分别转染空载质粒、转染206过表达质粒、转染空载质粒或206过表达质粒后加入表皮生长因子(EGF)诱导细胞上皮-间质转化(EMT)发生。观察细胞形态改变。采用Western blotting检测TMEM206及EMT相关蛋白的表达,采用Transwell实验分析结直肠癌细胞的侵袭、迁移能力。结果TMEM206过表达促进EGF诱导的EMT样细胞形态。Western blotting结果显示,TMEM206过表达促进了EGF诱导的p-ERK和c-Myc蛋白增加(P<0.05),并促进EGF诱导的E-钙黏蛋白减少以及纤连蛋白、Zeb1、Snail1、Snail2增加(P<0.05)。Transwell结果显示,HCT116和SW480细胞过表达TMEM206后,进一步促进了EGF诱导后细胞侵袭、迁移能力的增强(P<0.05)。结论TMEM206促进结直肠癌EMT发生,进而影响结直肠癌的侵袭、转移。

Objective To examine the role and underlying mechanism of TMEM206 in the development and progression of colorectal cancer.Methods Colorectal cancer cell lines,HCT116 and SW480,were randomly divided into four groups.The cells were transfected with vector and TMEM206-overexpressing plasmids,and then treated with epidermal growth factor(EGF)to induce epithelial-mesenchymal transition(EMT).The changes in the expression of TMEM206 and EMT-related proteins were detected by Western blotting.The invasion and migration ability of the colorectal cancer cells were analyzed using Transwell assays.Results TMEM206 overexpression promoted EGF-induced EMT-like cell morphology.Western blotting showed that TMEM206 overexpression promoted EGF-induced increase in the expression of p-ERK and c-Myc proteins(P<0.05),and it also promoted EGF-induced EMT,as indicated by the decrease in E-cadherin expression and increase in the expression of fibronectin,Zeb1,Snail1,and Snail2(P<0.05).The Transwell assays showed that TMEM206 overexpression further promoted the invasion and migration of the HCT116 and SW480 cells after EGF was induced(P<0.05).Conclusion TMEM206 promotes invasion and metastasis by regulating the development of EMT in colorectal cancer.