| First Author | Grill JI | Year | 2015 |
| Journal | Biochem Biophys Res Commun | Volume | 461 |
| Issue | 2 | Pages | 249-53 |
| PubMed ID | 25869068 | Mgi Jnum | J:228385 |
| Mgi Id | MGI:5706885 | Doi | 10.1016/j.bbrc.2015.04.009 |
| Citation | Grill JI, et al. (2015) Inactivation of Itf2 promotes intestinal tumorigenesis in Apc(Min/+) mice. Biochem Biophys Res Commun 461(2):249-53 |
| abstractText | Deregulation of Wnt/beta-catenin signaling following inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene is frequently found in colorectal cancer. We have previously shown that levels of ITF-2B, encoded by the beta-catenin target gene ITF2 that is located on the tumor suppressor gene locus 18q21, are increased in colonic adenomas with deregulated beta-catenin activity. However, during tumor progression ITF-2B levels are reduced, suggesting that ITF-2B interferes with tumor development. To investigate the role of ITF2 in intestinal tumorigenesis, we specifically inactivated Itf2 in the intestinal epithelium of Apc(Min/+) mice. We found that genetic disruption of Itf2 on the Apc(Min/+) background results in earlier death and a significant increase in tumor number and size in the small intestine. Based on these data Itf2 acts as a tumor suppressor gene of the intestinal tract that inhibits tumor initiation and growth. |
