目的:研究TGF-β1上调MTA1能否促进人舌癌Tca8113细胞侵袭转移。方法:蛋白印迹和实时定量PCR检测TGF-β1刺激或者不刺激的Tca8113细胞中MTA1和E-cadherin的表达。β-actin作为实验的内参对照。光学显微镜拍摄TGF-β1刺激的Tca8113细胞形态。侵袭实验检测TGF-β1刺激的Tca8113细胞。结果:TGF-β1上调MTA1蛋白和mRNA表达,下调E-cadherin表达水平。Tca8113细胞是呈多边形的口腔鳞状上皮细胞癌,经TGF-β1刺激的Tca8113细胞形态变成长梭形。同时,TGF-β1刺激的Tca8113细胞与对照相比较具有更强的侵袭能力。结论:TGF-β1信号能通过MTA1下调E-cadherin表达,这可能是促进舌癌侵袭和转移的机制之一。
Objective:We investigated the effects of TGF- β1 to upregulate MTA1 on invasion and metastasis in human tongue Tca8115 cancer ceils. Methods: Western blot and real- time PCR analysis were used to detect for MTA1 and E- cadherin expression from the cell lysates isolated from TcaSll3 cells treated with and without TGF- β1.β -actin was used as the loading control. Bright -phase microscopic analyzed Tca8113 treated with and without TGF - β1. Tca8113 cells were used in migration assay in the presence and absence of TGF -β1. Results:TGF - β1 upregulated the expression of MTA1 protein and mRNA and downregulated the level of E - cadherin. TcaS1β cells were oral squamous epithelial cell carcinoma with polygonal morphology while TGF - β1 stimulated its trans - differ- entiation into mesenchymal phenotype with an elongated morphology. Furthermore, the assay showed that the Tca8113/ TGF - β1 ceils had greater migration ability than the control cells. Conclusion:MTA1 in the regulation of TGF - β1 -mediated E -cadherin repression,which may be one of the mechanisms that attributes to the motility, invasion and metastatic potential of tongue cancer cell.