ArticleThe Journal of clinical investigation2023
Claudin-2 protects against colitis-associated cancer by promoting colitis-associated mucosal healing.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Modulation of intestinal bile acids influences colonic mucosal responses.Scientific reports · 2026Article
- Betanin ameliorates dextran sulfate sodium-induced colitis in mice by modulating tight junction protein expression.Biochemistry and biophysics reports · 2026Article
- CRISPR/Cas9-mediated claudin-2 knockout in HCT116 cells reveals its key role in colorectal cancer progression.Oncology letters · 2026Article
- Resveratrol-embedded hollow cerium oxide nanomedicine targeted treat inflammatory bowel disease through ROS clearance, intestinal mucosal immune homeostasis recovery and gut microbiota modulation.Materials today. Bio · 2026Article
- GLP-1 and GLP-2 as intestinal reparative therapies in inflammatory bowel disease: mechanisms, translation, and clinical opportunity.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- Integrative transcriptomic profiling and machine learning reveal hypoxia-associated molecular signatures for precision diagnosis in thyroid eye disease.Human genomics · 2025Article
- Genomic and functional characterization of amSystems · 2025Article
- Importance of rectal over colon status in ulcerative colitis remission: the role of microinflammation and mucosal barrier dysfunction in relapse.Journal of gastroenterology · 2025Article
- Machine Learning and Mendelian Randomization Identify Six Cell Death-Related Genes Driving Ulcerative Colitis Progression and Treatment Response.Journal of inflammation research · 2025Article
- Duodenal Organoids From Metabolic Dysfunction-Associated Steatohepatitis Patients Exhibit Absorptive and Barrier Alterations.Gastro hep advances · 2025Article
- Targeting the Calcium-Sensing Receptor in Chemically Induced Medium-Grade Colitis in Female BALB/C Mice.Nutrients · 2024Article
- Unveiling the Immune effects of AHR in tumors: a decade of insights from bibliometric analysis (2010-2023).Discover oncology · 2024Article
- Changes in the Expression of Genes Regulating the Response to Hypoxia, Inflammation, Cell Cycle, Apoptosis, and Epithelial Barrier Functioning during Colitis-Associated Colorectal Cancer Depend on Individual Hypoxia Tolerance.International journal of molecular sciences · 2024Article
- Claudin-2 upregulation enhances intestinal permeability, immune activation, dysbiosis, and mortality in sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Molecular cross-talk among human intestinal bifidobacteria as explored by a human gut model.Frontiers in microbiology · 2024Article
- Identification of claudin-2 as a promising biomarker for early diagnosis of pre-diabetes.Frontiers in pharmacology · 2024Article
- Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Patients with inflammatory bowel disease (IBD) are susceptible to colitis-associated cancer (CAC). Chronic inflammation promotes the risk for CAC. In contrast, mucosal healing predicts improved prognosis in IBD and reduced risk of CAC. However, the molecular integration among colitis, mucosal healing, and CAC remains poorly understood. Claudin-2 (CLDN2) expression is upregulated in IBD; however, its role in CAC is not known. The current study was undertaken to examine the role for CLDN2 in CAC. The AOM/DSS-induced CAC model was used with WT and CLDN2-modified mice. High-throughput expression analyses, murine models of colitis/recovery, chronic colitis, ex vivo crypt culture, and pharmacological manipulations were employed in order to increase our mechanistic understanding. The Cldn2KO mice showed significant inhibition of CAC despite severe colitis compared with WT littermates. Cldn2 loss also resulted in impaired recovery from colitis and increased injury when mice were subjected to intestinal injury by other methods. Mechanistic studies demonstrated a possibly novel role of CLDN2 in promotion of mucosal healing downstream of EGFR signaling and by regulation of Survivin expression. An upregulated CLDN2 expression protected from CAC and associated positively with crypt regeneration and Survivin expression in patients with IBD. We demonstrate a potentially novel role of CLDN2 in promotion of mucosal healing in patients with IBD and thus regulation of vulnerability to colitis severity and CAC, which can be exploited for improved clinical management.
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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.