转录因子FOXC1促进胶质瘤细胞系U87的侵袭能力

目的：探讨转录因子FOXC1对人脑胶质瘤细胞系U87侵袭的促进作用。方法：qPCR、Western blot检测胶质瘤细胞系U87、U251及正常星型胶质细胞中FOXC1 mRNA和蛋白表达水平。将FOXC1-siRNA转染至U87细胞中，分别用qPCR、Western blot检测FOXC1-siRNA的转染效率。细胞划痕实验和Transwell实验检测U87细胞转染FOXC1-siRNA后对细胞侵袭能力的影响，利用 Western blot检测U87细胞上皮间质化相关通路蛋白（Snail1、β-catenin、Twist1）、标记蛋白（N-cadherin、Vimentin、E-cadherin）表达水平。结果：U87细胞下调FOXC1表达后侵袭能力明显减弱，上皮间质化相关通路蛋白（Snail1、β-catenin、Twist1）表达水平下降，上皮细胞标记蛋白表达水平E-cadherin表达水平升高、间质细胞标记蛋白N-cadherin、Vimentin表达水平降低。结论：转录因子FOXC1通过上皮间质化促进胶质瘤细胞的侵袭。

Effects of FOXC1 on invasion of glioblastoma U87 cells

Objective: To explore the promotive effect of FOXC1 on the invasion of glioblastoma U87 cells. Methods: The mRNA and protein expression levels of endogenous FOXC1 was examined in U87 and U251 cells as well as NHAs via qPCR and Western blot, respectively. The FOXC1-siRNA was transfected into U87 cells. The transfection efficacy of FOXC1-siRNA was examined using qPCR and Western blot. The wound healing assay and Transwell invasion assay were carried out to investigate the role of FOXC1 on glioma cell invasion. The changes of epithelial-mesenchymal transition(EMT)-related signaling pathway proteins and marker proteins in glioma cells were identified with Western blot. Results: Downregulating the expression of FOXC1 reduced the invasive ability of glioma cells, reduced the EMT-related signaling pathway proteins of glioma cells, increased the epithelial biomarker E-cadherin and decreased the mesenchymal biomarkers N-cadherin and Vimentin. Conclusion: The FOXC1 could effectively promote the invasion of glioma cells by inducing EMT.