ArticleThe Journal of clinical investigation2018
Claudin-18-mediated YAP activity regulates lung stem and progenitor cell homeostasis and tumorigenesis.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 188 citations in OpenAlex.
- Cell differentiation-related signaling pathways: biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- TP53/TAU axis regulates microtubule bundling to control alveolar stem cell-mediated regeneration.The Journal of clinical investigation · 2026Article
- Molecular imaging in gastric cancer: state-of-the-art techniques and emerging opportunities.Journal of translational medicine · 2026Review
- Single-nucleus multi-omics delineates distinct epigenetic programs associated with tumor progression in lung adenocarcinoma.Clinical epigenetics · 2026Article
- Genome-wide CRISPR screening identifiesOncology letters · 2026Article
- Review
- FAM189A2 activates Hippo signaling pathway by abrogating WWP2-mediated LATS1 ubiquitination, to inhibit the glycolysis and proliferation processes of lung adenocarcinoma.Journal of translational medicine · 2025Article
- Investigating the role of oncogenic FAM83A as a prognostic biomarker in lung adenocarcinoma: Insights from smoker and non-smoker cohorts.Journal, genetic engineering & biotechnology · 2025Article
- Functional landscape of mechanistic diversity in 27 claudin family members at tight junctions.Science advances · 2025Article
- Targeting Claudin18.2 for cancer theranostics: From molecular imaging to precision therapy.iScience · 2025Review
- Distal lung organoids derived from adult stem cells as novel tools in deciphering mechanisms of lung regeneration, infection, and cancer.Stem cells translational medicine · 2025Review
- A Novel Tight Junction-Nuclear Receptor Signaling Pathway Regulating Cancer Progression.Pathology international · 2025Review
- Scaffolding Protein ENH Promotes Tumor Angiogenesis and Growth Through Macrophage Recruitment and Polarization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Yes-associated protein induces age-dependent inflammatory signaling in the pulmonary endothelium.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Claudin-1 Contributes to Gastrointestinal Stromal Tumors (GIST) Resistance to Imatinib Mesylate (IM) via Regulation of FGFR-Signaling.International journal of molecular sciences · 2025Article
- Prognostic role of claudin-18.2 in intrahepatic cholangiocarcinoma.Virchows Archiv : an international journal of pathology · 2025Article
- Inhibition of DLK1 regulates AT2 differentiation and alleviates established pulmonary fibrosis by upregulating TTF-1/CLDN6.Respiratory research · 2025Article
- Yes-associated Protein Induces Age-dependent Inflammatory Signaling in the Pulmonary Endothelium.bioRxiv : the preprint server for biology · 2025Article
- Article
48 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 4 institutions in 3 countries.
Funding
Abstract
Claudins, the integral tight junction (TJ) proteins that regulate paracellular permeability and cell polarity, are frequently dysregulated in cancer; however, their role in neoplastic progression is unclear. Here, we demonstrated that knockout of Cldn18, a claudin family member highly expressed in lung alveolar epithelium, leads to lung enlargement, parenchymal expansion, increased abundance and proliferation of known distal lung progenitors, the alveolar epithelial type II (AT2) cells, activation of Yes-associated protein (YAP), increased organ size, and tumorigenesis in mice. Inhibition of YAP decreased proliferation and colony-forming efficiency (CFE) of Cldn18-/- AT2 cells and prevented increased lung size, while CLDN18 overexpression decreased YAP nuclear localization, cell proliferation, CFE, and YAP transcriptional activity. CLDN18 and YAP interacted and colocalized at cell-cell contacts, while loss of CLDN18 decreased YAP interaction with Hippo kinases p-LATS1/2. Additionally, Cldn18-/- mice had increased propensity to develop lung adenocarcinomas (LuAd) with age, and human LuAd showed stage-dependent reduction of CLDN18.1. These results establish CLDN18 as a regulator of YAP activity that serves to restrict organ size, progenitor cell proliferation, and tumorigenesis, and suggest a mechanism whereby TJ disruption may promote progenitor proliferation to enhance repair following injury.
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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.