ArticleBiochimica et biophysica acta. Molecular basis of disease2022
GPR65 (TDAG8) inhibits intestinal inflammation and colitis-associated colorectal cancer development in experimental mouse models.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 33 citations in OpenAlex.
- Unveiling the impact of colonic pH and pH-sensing receptors in blood pressure regulation.Gut microbes · 2026Review
- Loss of proton-sensing TDAG8 increases tumor progression in mouse models of colon cancer.Molecular oncology · 2026Article
- Novel preparation of pH-responsive hydrogel with chitosan-based microbeads for targeted oral delivery of bevacizumab to enhanced apoptosis in azoxymethane-induced colorectal cancer: cellular and in vivo mice models.Drug delivery and translational research · 2026Article
- GPR65 as a Laryngeal Cancer Risk Gene Identified through Single-Cell Transcriptomics, Mendelian Randomization Analysis, and Experimental Validation.Anti-cancer agents in medicinal chemistry · 2026Article
- Orphan GPCRs in diabetes mellitus: metabolic control, inflammation, and drug development.Frontiers in endocrinology · 2026Review
- Low pH, High Stakes: A Narrative Review Exploring the Acid-Sensing GPR65 Pathway as a Novel Approach in Renal Cell Carcinoma.Cancers · 2025Review
- GPR65 is a novel immune biomarker and regulates the immune microenvironment in lung adenocarcinoma.Frontiers in immunology · 2025Article
- Integrating single-cell sequencing and transcriptome analysis to unravel the mechanistic role of sialylation-related genes in sepsis-induced acute respiratory distress syndrome.Frontiers in immunology · 2025Article
- Macrophages make "sense" of obesity-driven acidity in the TME.Cell chemical biology · 2024Article
- Inflammatory bowel disease, colitis, and cancer: unmasking the chronic inflammation link.International journal of colorectal disease · 2024Review
- Review
- Small-molecule probe for IBD risk variant GPR65 I231L alters cytokine signaling networks through positive allosteric modulation.Science advances · 2024Article
- Recent advances in acid sensing by G protein coupled receptors.Pflugers Archiv : European journal of physiology · 2024Review
- Role of pH-sensing receptors in colitis.Pflugers Archiv : European journal of physiology · 2024Review
- Proton-sensing ion channels, GPCRs and calcium signaling regulated by them: implications for cancer.Frontiers in cell and developmental biology · 2024Review
- Article
- OGR1 (GPR68) and TDAG8 (GPR65) Have Antagonistic Effects in Models of Colonic Inflammation.International journal of molecular sciences · 2023Article
- Expression of pH-Sensitive GPCRs in Peritoneal Carcinomatosis of Colorectal Cancer-First Results.Journal of clinical medicine · 2023Article
- GPR65 as a potential immune checkpoint regulates the immune microenvironment according to pan-cancer analysis.Heliyon · 2023Article
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
GPR65 (TDAG8) is a proton-sensing G protein-coupled receptor predominantly expressed in immune cells. Genome-wide association studies (GWAS) have identified GPR65 gene polymorphisms as an emerging risk factor for the development of inflammatory bowel disease (IBD). Patients with IBD have an elevated risk of developing colorectal cancer when compared to the general population. To study the role of GPR65 in intestinal inflammation and colitis-associated colorectal cancer (CAC), colitis and CAC were induced in GPR65 knockout (KO) and wild-type (WT) mice using dextran sulfate sodium (DSS) and azoxymethane (AOM)/DSS, respectively. Disease severity parameters such as fecal score, colon shortening, histopathology, and mesenteric lymph node enlargement were aggravated in GPR65 KO mice compared to WT mice treated with DSS. Elevated leukocyte infiltration and fibrosis were observed in the inflamed colon of GPR65 KO when compared to WT mice which may represent a cellular mechanism for the observed exacerbation of intestinal inflammation. In line with high expression of GPR65 in infiltrated leukocytes, GPR65 gene expression was increased in inflamed intestinal tissue samples of IBD patients compared to normal intestinal tissues. Moreover, colitis-associated colorectal cancer development was higher in GPR65 KO mice than WT mice when treated with AOM/DSS. Altogether, our data demonstrate that GPR65 suppresses intestinal inflammation and colitis-associated tumor development in murine colitis and CAC models, suggesting potentiation of GPR65 with agonists may have an anti-inflammatory therapeutic effect in IBD and reduce the risk of developing colitis-associated colorectal cancer.
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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.