Carcinogenesis, Vol 19, 543-549, Copyright © 1998 by Oxford University Press
H Sheng, J Shao, CS Williams, MA Pereira, MM Taketo, M Oshima, AB Reynolds, MK Washington, RN DuBois and RD Beauchamp
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.
ARTICLES
Nuclear translocation of beta-catenin in hereditary and carcinogen- induced intestinal adenomas
Department of Surgery, The Vanderbilt Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
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