An intestinal stem cell niche in Apc mutated neoplasia targetable by CtBP inhibition.

ABSTRACT: C-terminal binding protein 2 (CtBP2) drives intestinal polyposis in the Apc^min mouse model of human Familial Adenomatous Polyposis. As CtBP2 is targetable by an inhibitor of its dehydrogenase domain, understanding CtBP2's role in adenoma formation is necessary to optimize CtBP-targeted therapies in Apc mutated human neoplasia. Tumor initiating cell (TIC) populations were substantially decreased in Apc^minCtbp2^+/- intestinal epithelia. Moreover, normally nuclear Ctbp2 was mislocalized to the cytoplasm of intestinal crypt stem cells in Ctbp2^+/- mice, both Apc^min and wildtype, correlating with low/absent CD133 expression in those cells, and possibly explaining the

SUBMITTER: Chawla AT 

PROVIDER: S-EPMC6126694 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature