Loss of Stat6 affects chromatin condensation in intestinal epithelial cells causing diverse outcome in murine models of inflammation-associated and sporadic colon carcinogenesis.

ABSTRACT: While great advances have been achieved regarding the genetic basis of colorectal cancer, the complex role of cell-cell communication and cytokine-induced signaling during its pathogenesis remains less understood. Signal transducer and activator of transcription 6 (Stat6) is the main transcription factor of interleukin-4 (IL-4) signaling and its participation in the development of various tumor types has been already reported. Here we aimed to examine the contribution of Stat6 in intestinal epithelial cells (IEC) in mouse models of intestinal carcinogenesis. Wild-type (WT), Stat6 knockout (Stat6^-/-), and intestinal epithelial cell-specific IL-4Rα knockout (Il-4rα^ΔIEC) mice were subjected to colitis-associated (AOM/DSS) and colitis-independent (sporadic) carcinogenesis

SUBMITTER: De Oliveira T 

PROVIDER: S-EPMC6756235 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature