ArticleCell death & disease2020
Mutant CFTR Drives TWIST1 mediated epithelial-mesenchymal transition.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- Jinshui Liujun Decoction attenuates cigarette smoke-induced small airway remodeling via the TGF-β/Smad2/CFTR Axis.The journal of physiological sciences : JPS · 2026Article
- Cystic Fibrosis and Colorectal Cancer Risk: Reprogramming of the Intestinal Epithelial Niche and Cell-State Plasticity in the CFTR Modulator Era.Cell proliferation · 2026Review
- The Ion channel, CFTR, assembles with HIPPO pathway proteins TAZ and YAP in polycystic kidney disease.The Journal of biological chemistry · 2026Article
- Cx43 levels guide apicobasal polarity in regenerating airway epithelial cells.Communications biology · 2026Article
- Review
- Modulation of immune responses by elexacaftor/tezacaftor/ivacaftor therapy in cystic fibrosis: data from a compassionate use program.Respiratory research · 2026Article
- Cystic fibrosis airway epithelial cells have an exaggerated response to hypoxia that is partially reversible through transmembrane receptor modulation.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025Article
- Enrichment of Germline Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Pathogenic Variants in Patients With Solid Tumors: Evidence for Increased Cancer Risk.Pediatric pulmonology · 2025Article
- Inflammation and epithelial-mesenchymal transition in a CFTR-depleted human bronchial epithelial cell line revealed by proteomics and human organ-on-a-chip.The FEBS journal · 2025Article
- CF airway epithelia display exaggerated host defense responses and prolonged cilia loss during RSV infection.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025Article
- Identification of a vimentin-expressing α-cell phenotype in CF and normal pancreas.The Journal of endocrinology · 2025Article
- CFTR as a therapeutic target for severe lung infection.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- CFTR ion transport deficiency primes the epithelium for partial epithelial-mesenchymal transition in cystic fibrosis.Frontiers in pharmacology · 2025Article
- GABRP inhibits the progression of oesophageal cancer by regulating CFTR: Integrating bioinformatics analysis and experimental validation.International journal of experimental pathology · 2024Article
- Disrupting the TGF-β-Wnt Balance to Control the Polarity of the Cystic Fibrosis Airway Epithelium.American journal of respiratory cell and molecular biology · 2024Article
- Apical dehydration impairs the cystic fibrosis airway epithelium barrier via aLife science alliance · 2024Article
- Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on ClInternational journal of molecular sciences · 2023Review
- Intercellular Communication in Airway Epithelial Cell Regeneration: Potential Roles of Connexins and Pannexins.International journal of molecular sciences · 2023Review
- Roles of Twist1 in lipid and glucose metabolism.Cell communication and signaling : CCS · 2023Review
- The epithelial-mesenchymal plasticity landscape: principles of design and mechanisms of regulation.Nature reviews. Genetics · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic fibrosis (CF) is a monogenetic disease resulting from mutations in the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) gene encoding an anion channel. Recent evidence indicates that CFTR plays a role in other cellular processes, namely in development, cellular differentiation and wound healing. Accordingly, CFTR has been proposed to function as a tumour suppressor in a wide range of cancers. Along these lines, CF was recently suggested to be associated with epithelial-mesenchymal transition (EMT), a latent developmental process, which can be re-activated in fibrosis and cancer. However, it is unknown whether EMT is indeed active in CF and if EMT is triggered by dysfunctional CFTR itself or a consequence of secondary complications of CF. In this study, we investigated the occurrence of EMT in airways native tissue, primary cells and cell lines expressing mutant CFTR through the expression of epithelial and mesenchymal markers as well as EMT-associated transcription factors. Transepithelial electrical resistance, proliferation and regeneration rates, and cell resistance to TGF-β1induced EMT were also measured. CF tissues/cells expressing mutant CFTR displayed several signs of active EMT, namely: destructured epithelial proteins, defective cell junctions, increased levels of mesenchymal markers and EMT-associated transcription factors, hyper-proliferation and impaired wound healing. Importantly, we found evidence that the mutant CFTR triggered EMT was mediated by EMT-associated transcription factor TWIST1. Further, our data show that CF cells are over-sensitive to EMT but the CF EMT phenotype can be reversed by CFTR modulator drugs. Altogether, these results identify for the first time that EMT is intrinsically triggered by the absence of functional CFTR through a TWIST1 dependent mechanism and indicate that CFTR plays a direct role in EMT protection. This mechanistic link is a plausible explanation for the high incidence of fibrosis and cancer in CF, as well as for the role of CFTR as tumour suppressor protein.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.