ArticleJournal of Crohn's & colitis2025
T-cell branched glycosylation as a mediator of colitis-associated colorectal cancer progression: a potential new risk biomarker in inflammatory bowel disease.
Article in Journal of Crohn's & colitis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Potential role of PPARGC1A in linking ulcerative colitis to colorectal cancer: a novel prognostic biomarker and therapeutic target.Translational cancer research · 2026Article
- Mucosal glycans: key drivers of the development of inflammatory bowel disease and a potential new therapeutic target.Nature reviews. Gastroenterology & hepatology · 2026Review
- Post-Translational Regulation of CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Stromal ARHGEF15 Correlates With Inflammatory EMT and Stromal-Immune Crosstalk During Inflammatory Bowel Disease-To-Colorectal Cancer Progression.Bioinformatics and biology insights · 2026Article
- Reprogramming CD8+ T-cell Branched N-Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing.Cancer immunology research · 2025Article
- Tumor glyco-immunology, glyco-immune checkpoints and immunotherapy.Journal for immunotherapy of cancer · 2025Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
BACKGROUND AND
aimsInflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract, established as a risk factor for colorectal cancer (CRC) development. Long-standing inflammation appears to play a central role in colitis-associated colorectal cancer (CAC). However, the molecular mechanism underlying CAC progression is still elusive. Previous evidence showed that levels of branched glycosylation regulate T-cell-mediated immune response associated with IBD severity. Here, we revealed that colonic T cells from IBD patients are dynamically regulated by branched N-glycosylation and associated with the risk of CAC development.
methodsWe performed in silico analysis for glycome and immune profile of a publicly available human dataset of CAC patients. Additionally, in a well-characterized cohort of CAC patients, we evaluated the N-glycosylation profile of infiltrated colonic immune cells at different stages of carcinogenesis (colitis, dysplasia and cancer). In vivo studies were conducted in Mgat5 KO mice, using AOM/DSS model to induce CAC. Tumor development and colonic T cells glycoprofile were characterized during CAC development.
resultsThe combined analysis of human IBD and CAC clinical samples, together with glycoengineered mouse model susceptible to CAC, revealed a gradual and dynamic increase of branched N-glycans in T cells from colitis to dysplasia and cancer. This glycosylation switch was shown to impose inhibitory properties in T cells, precluding an effective antitumor immune response. Mechanistically, we demonstrated that the deletion of branched N-glycans in Mgat5 knockout mice led to CAC suppression due to increased infiltration of CD8+and γδ T cells, contributing to an effective antitumor immune response. From the clinical standpoint, we demonstrated that branched N-glycosylation levels detected in inflamed lesions from IBD patients predicted CAC progression with a sensitivity of 83.3% and specificity of 67.9% when assessed together with age at diagnosis.
conclusionsOverall, we here disclosed a new mechanism underlying CAC development, identifying a potential clinical biomarker plausible to improve the efficacy of cancer surveillance programs through the early identification of high-risk IBD patients, for preventive clinical and therapeutic strategies.
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