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Effect of TRIB3 overexpressing on the gene expression in NCM460 cells

ABSTRACT: Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is a chronic and relapsing disorder with increased prevalence all over the world. Bile acids are small molecules synthesized from cholesterol by the liver, and their metabolic disorder has a positive correlation with IBD development. Here, we identified that GCA promotes DSS induced mouse colitis through downregulating Tribbles homolog 3 (TRIB3) to inhibit the function of intestinal stem cells, which suggested the potential harmful biological function of conjugated primary bile acid—GCA in IBD. Then we have demonstrated that TRIB3 is highly expressed in crypts, to maintain the ISCs stemness traits. Downregulation of TRIB3 in intestinal epithelium cells accelerated IBD progression. To decipher the molecular mechanisms of TRIB3 in maintaining intestinal stem cells renewal, we established the control and TRIB3 overexpressing NCM460 cells to perform this high-throughput mRNA sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE276541 | GEO | 2026/05/03

REPOSITORIES: GEO

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Comprehensive Profiling of Mammalian Tribbles Interactomes Implicates TRIB3 in Gene Repression

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