ArticleExperimental and therapeutic medicine2023
FOXF1 attenuates TGF‑β1‑induced bronchial epithelial cell injury by inhibiting CDH11‑mediated Wnt/β‑catenin signaling.
Article in Experimental and therapeutic medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- A positive feedback loop between CDH11 and TGF-β signaling regulates migration and invasion of gastric cancer.Translational oncology · 2026Article
- Identification and Characterisation of Canine Osteosarcoma Biomarkers and Therapeutic Targets.Cancers · 2026Article
- Single-cell transcriptomic analysis of the heterogeneity of mesenchymal and stromal cells and their regulon alteration during airway remodeling in asthma.Scientific reports · 2025Article
- Integrative multi-omics analysis reveals key regulatory nodes of abdominal fat deposition in broiler chickens.Poultry science · 2025Article
- Cloning and Transcriptional Activity Analysis of the BovineAnimals : an open access journal from MDPI · 2025Article
- GTX-11 attenuates lung fibrosis, inflammation and vascular remodeling in preclinical models of lung fibrotic disease.Frontiers in pharmacology · 2025Article
- Tangeretin attenuates bleomycin-induced pulmonary fibrosis by inhibiting epithelial-mesenchymal transition via the PI3K/Akt pathway.Frontiers in pharmacology · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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, 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/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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