T-cell branched glycosylation as a mediator of colitis-associated colorectal cancer progression: a potential new risk biomarker in inflammatory bowel disease.

ABSTRACT:

Background and aims

Inflammatory 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.

Methods

We performed in silico analysis for glycome and immune profile of a publicly available human dataset of CAC pat

SUBMITTER: Leite-Gomes E 

PROVIDER: S-EPMC12032605 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature