Nuclear translocation of beta-catenin in hereditary and carcinogen-induced intestinal adenomas.

Sheng H, Shao J, Williams CS, Pereira MA, Taketo MM, Oshima M, Reynolds AB, Washington MK, DuBois RN, Beauchamp RD
Carcinogenesis. 1998 19 (4): 543-9

PMID: 9600336 · DOI:10.1093/carcin/19.4.543

The physical interaction between beta-catenin and the adenomatous polyposis coli (APC) gene, and the ability of APC to regulate cytoplasmic levels of beta-catenin suggest a role for beta-catenin in colorectal carcinogenesis. In this study, we found that beta-catenin immunoreactivity was detected exclusively in the cell membrane and cytoplasm of morphologically normal intestinal epithelial cells with predominant distribution in the differentiated nonproliferative cell population. In contrast, beta-catenin was localized predominantly in the nucleus of adenomas from Min/+ mice and transgenic mice expressing a mutant truncated form of the APC gene (Apc(delta716) mice). Beta-catenin was expressed predominantly at the cell membrane and cytoplasm of the nontransformed rat intestinal epithelial (RIE-1) cells in culture, whereas predominantly nuclear localization of beta-catenin was observed in the human colon cancer cell line SW480. In the azoxymethane (AOM) treated rats, overexpression and nuclear localization of beta-catenin was observed in all adenomas. Previous studies have indicated the incidence of APC mutations amongst AOM-induced tumors to be 15% or less. These results demonstrate that nuclear localization of beta-catenin is a common event in colorectal tumorigenesis.

MeSH Terms (19)

Adenoma Animals Azoxymethane beta Catenin Biological Transport Carcinogens Cell Nucleus Cytoskeletal Proteins Epithelial Cells Female Genes, APC Humans Intestinal Neoplasms Male Mice Mice, Transgenic Rats Trans-Activators Tumor Cells, Cultured

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