Beta-Catenin stabilization imparts crypt progenitor phenotype to hyperproliferating colonic epithelia.

ABSTRACT: Utilizing the Citrobacter rodentium (CR)-induced transmissible murine colonic hyperplasia (TMCH) model, we provide mechanistic basis of changes in beta-catenin/APC/CKIepsilon leading to progression and/or regression of hyperplasia in vivo. In response to CR-induced TMCH, crypt lengths increased significantly between days 6-27 post-infection, followed by a steep decline by day 34. beta-Cat(45)/total beta-catenin were elevated on day 1 post-infection, preceding changes in crypt length, and persisted for 27 days before declining by day 34. Importantly, cellular CKIepsilon and beta-catenin co-immunoprecipitated and exhibited remarkable parallel changes in kinetics during hyperplasia/regression phases. beta-catenin, phosphorylated at Ser33,37 and Thr41 (beta-cat(33,37/41)), was low till day 12,

SUBMITTER: Sellin JH 

PROVIDER: S-EPMC2868370 | biostudies-literature | 2009 Jan

REPOSITORIES: biostudies-literature