Retinoid acid induced 16 deficiency aggravates colitis and colitis-associated tumorigenesis in mice.

ABSTRACT: Inflammatory bowel disease (IBD) and colitis-associated colorectal cancer (CAC) is a serious health issue, but etiopathological factors remain unclear. Although some studies reported the roles of Retinoid acid induced 16 (RAI16) in the tumorigenesis of hepatocellular carcinoma and PKA signaling, the roles of RAI16 in IBD and CRC are undressed. RAI16^-/- mice were generated and the roles of RAI16 were addressed in dextran sodium sulfate (DSS) or azoxymethane (AOM)-DSS induced IBD or CAC mouse models, respectively. At first, RAI16^-/- mice were viable, fertile with no apparent defects. Then, it was found that RAI16^-/- mice were more susceptibility to colitis induced by DSS than wild type (WT) littermates, which was evaluated by disease activity index and histol

SUBMITTER: Xu YL 

PROVIDER: S-EPMC6925230 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature