Tgf-Beta Participates In Epithelial-Mesenchymal Transition In Pleural Fibrosis Via Targeting S100a4

TGF-β-induced EMT participates in fibrosis. S100A4 is a target of TGF-β signaling. Previously, we have reported S100A4 is highly expressed in pleural fibrosis. Thus, we hypothesized that S100A4 took part in the TGF-β-induced EMT in pleural fibrosis. In this study, we detected the expression of S100A4, EMT- and ECM-related markers in Met-5A cells treated with TGF-β or TGF-β inhibitor by real-time PCR, western blot and ELISA. In order to explore the role of S100A4, we used siRNA to knock down the expression of S100A4 in cell model. We found the expression of epithelial cell marker was decreased and the mesenchymal cell marker increased with ECM deposition and S100A4 up-regulation after treatment with TGF-β. Moreover, the changes of EMT-related event were restricted when the expression of S100A4 was knocked down. Conversely, S100A4 can partially rescue the EMT-related expression changes induced by TGF-β inhibitor. These findings suggest that S100A4 expression is induced by the TGF-β pathway and silencing S100A4 expression can inhibit the process of TGF-β- induced EMT, what might pave the way for new and effective treatment for pleural fibrosis.