FOXF1 attenuates TGF‑β1‑induced bronchial epithelial cell injury by inhibiting CDH11‑mediated Wnt/β‑catenin signaling

Abstract

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 β1 (TGF-β1)-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-β1-induced bronchial epithelial cells. Proliferation, apoptosis and inflammation were assessed using Cell Counting Kit-8 assay, f low 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/β-catenin pathway were detected by western blotting. The results indicated that FOXF1 expression was downregulated, while CDH11 expression was upregulated in TGF-β1-treated BEAS-2B cells. FOXF1 overexpression promoted proliferation, inhibited induction of apoptosis and suppressed the inflammatory response of BEAS-2B cells exposed to TGF-β1. In addition, FOXF1 overexpression restrained TGF-β1-induced bronchial epithelial fibrosis and EMT and inhibited the activation of the Wnt/β-catenin pathway. CDH11 overexpression reversed the effects of FOXF1 overexpression on proliferation, apoptosis, fibrosis, EMT and inflammation by regulating the Wnt/β-catenin pathway. Collectively, the results of the present study suggested that FOXF1 regulated TGF-β1-induced BEAS-2B cell injury by inhibiting CDH11-mediated Wnt/β-catenin signaling. This may provide a novel therapeutic strategy for the treatment of asthma.

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“…A549 cells were used to induce the phenotypic transformation caused by TGF-β1 and Western blotting was employed to analyze the effect of Tan on the epithelial-mesenchymal transition (EMT) phenotype The results indicated that consistent with previous studies, E-cadherin levels decreased and collagen I, N-cadherin, and α-SMA expression increased after TGF-β1 treatment, but improved after treatment with Tan(Q. Chen et al, 2023 ). Therefore, the research demonstrated that Tan can suppress EMT and inhibit pulmonary fibrosis.…”

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“…Regulation of MAPK kinases upstream of p38, the human mitogen-activated protein kinase kinase (MKK), such as MKK6 and MKK1, could selectively block the production of MMPs and pro-inflammatory cytokines in FLS (Hammaker et al, 2012). In addition, ubiquitin D might be considered a possible therapeutic target for RA-FLS (Chen et al, 2023).…”