Journal Article

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

H Sheng, J Shao, C S Williams, M A Pereira, M M Taketo, M Oshima, A B Reynolds, M K Washington, R N DuBois and R D Beauchamp

in Carcinogenesis

Volume 19, issue 4, pages 543-549
Published in print April 1998 | ISSN: 0143-3334
Published online April 1998 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/19.4.543
Nuclear translocation of beta-catenin in hereditary and carcinogen-induced intestinal adenomas.

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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.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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