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

Hongmiao Sheng, Jinyi Shao, Christopher S. Williams, Michael A. Pereira, Makoto M. Taketo, Masanobu Oshima, Albert B. Reynolds, Mary K. Washington, Raymond N. DuBois, R. Daniel Beauchamp

    Research output: Contribution to journalArticlepeer-review

    73 Scopus citations

    Abstract

    The physical interaction between β-catenin and the adenomatous polyposis coli (APC) gene, and the ability of APC to regulate cytoplasmic levels of β-catenin suggest a role for β-catenin in colorectal carcinogenesis. In this study, we found that β-catenin immunoreactivity was detected exclusively in the cell membrane and cytoplasm of morphologically normal intestinal epithelial cells with predominant distribution in the differentiated non-proliferative cell population. In contrast, β-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(Δ716) mice). β-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 β-catenin was observed in the human colon cancer cell line SW480. In the azoxymethane (AOM) treated rats, overexpression and nuclear localization of β-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 β-catenin is a common event in colorectal tumorigenesis.

    Original languageEnglish (US)
    Pages (from-to)543-549
    Number of pages7
    JournalCarcinogenesis
    Volume19
    Issue number4
    DOIs
    StatePublished - Apr 1998

    ASJC Scopus subject areas

    • Cancer Research

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