B-catenin deficiency, but not c-Myc deletion, suppresses the immediate phenotypes of Apc loss in the liver

ABSTRACT: Dysregulated Wnt signalling is seen in approximately 30% of hepatocellular cancers, thus finding pathways downstream of activation of Wnt signalling is key. Using cre lox technology we have deleted the the adenomatous polyposis coli tumour suppressor protein (Apc) within the adult mouse liver and observed a rapid increase in nuclear beta-catenin and C-Myc. This is associated with an induction of proliferation leading to hepatomegally within 4 days of gene deletion. To investigate the downstream pathways responsible for these phenotypes we analysed the impact of inactivating Apc in the context of deficiency of the potentially key effectors beta-catenin and c-Myc. beta-catenin loss rescues both the proliferation and hepatomegally phenotypes following Apc loss. However c-Myc deletion, which r

ORGANISM(S): Mus musculus

SUBMITTER: Karen Reed 

PROVIDER: E-GEOD-65476 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress