Format

Send to

Choose Destination
Biochem Biophys Res Commun. 2015 May 29;461(2):249-53. doi: 10.1016/j.bbrc.2015.04.009. Epub 2015 Apr 11.

Inactivation of Itf2 promotes intestinal tumorigenesis in Apc(Min/+) mice.

Author information

1
Department of Medicine II, University of Munich, 81377 Munich, Germany; Institute of Molecular Animal Breeding and Biotechnology, Gene Center, University of Munich, 81377 Munich, Germany. Electronic address: grill@genzentrum.lmu.de.
2
Department of Medicine II, University of Munich, 81377 Munich, Germany.
3
Institute of Pathology, University of Munich, 80337 Munich, Germany.
4
Institute of Molecular Animal Breeding and Biotechnology, Gene Center, University of Munich, 81377 Munich, Germany.
5
Department of Medicine II, University of Munich, 81377 Munich, Germany; German Cancer Consortium (DKTK), 69120 Heidelberg, Germany; German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany; Department of Internal Medicine and Gastroenterology, HELIOS Klinikum Berlin-Buch, Berlin, Germany.

Abstract

Deregulation of Wnt/β-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 β-catenin target gene ITF2 that is located on the tumor suppressor gene locus 18q21, are increased in colonic adenomas with deregulated β-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.

KEYWORDS:

Apc(Min/+) mouse; ITF2; Intestinal cancer

PMID:
25869068
DOI:
10.1016/j.bbrc.2015.04.009
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center