Abstract:Objective:To explore the effect of c-FLIP(L) in pulmonary fibrosis and its pathological mechanism. Methods: Based on bleomycin(BLM)induced idiopathic pulmonary fibrosis in mice, the expressions of c-FLIP and E-cadherin were analyzed by IHC staining. Further investigations in A549 cells overexpressing c-FLIP(L), the expression levels of E-cadherin, N-cadherin and Vimentin mRNA were examined by qRT-PCR, and Smad activation induced by TGF-β1 was detected by luciferase reporter assay and Western blot. Results: The increased c-FLIP expression was observed and associated with a decrease of E-cadherin expression. C-FLIP(L) overexpression resulted in the changes on E-cadherin, N-cadherin and Vimentin expressions in A549 cells. Furthemore, overexpression of c-FLIP(L) enhanced TGF-β-induced Smad activation, and knocking down c-FLIP(L) blocked the TGF-β1-induced EMT progress. Conclusion: C-FLIP(L) may be a promoting factor in the development of fibrosis via regulating EMT progress.