FOXF1 attenuates TGF-1-induced bronchial epithelial cell injury by inhibiting CDH11-mediated Wnt/-catenin signaling

Forkhead box F1 ( FOXF1) has been reported to be associated with lung development. However, the role of FOXF1 in asthma is still not fully understood. In the present study, the biological role and the potential mechanism of FOXF1 was explored in transforming growth factor beta 1 ( TGF-beta 1) -induced bronchial epithelial cell injury. Reverse transcription-quantitative PCR and western blotting were performed to detect the expression levels of FOXF1 and cadherin (CDH) 11 in TGF-beta 1-induced bronchial epithelial cells. Proliferation, apoptosis and inflammation were assessed using Cell Counting Kit-8 assay, flow cytometry, western blotting and ELISA. Fibrosis and epithelial-mesenchymal transition ( EMT) were evaluated using immunofluorescence and western blotting. The expression levels of the proteins involved in the Wnt/beta-catenin pathway were detected by western blotting. The results indicated that FOXF1 expression was downregulated, while CDH11 expression was upregulated in TGF-beta 1-treated BEAS-2B cells. FOXF1 overexpression promoted proliferation, inhibited induction of apoptosis and suppressed the inflammatory response of BEAS-2B cells exposed to TGF-beta 1. In addition, FOXF1 overexpression restrained TGF-beta 1-induced bronchial epithelial fibrosis and EMT and inhibited the activation of the Wnt/beta-catenin pathway. CDH11 overexpression reversed the effects of FOXF1 overexpression on proliferation, apoptosis, fibrosis, EMT and inflammation by regulating the Wnt/beta-catenin pathway. Collectively, the results of the present study suggested that FOXF1 regulated TGF-beta 1-induced BEAS-2B cell injury by inhibiting CDH11-mediated Wnt/beta-catenin signaling. This may provide a novel therapeutic strategy for the treatment of asthma.