What can humans learn from flies about adenomatous polyposis coli

被引:10
作者
Barth, AIM [1 ]
Nelson, WJ [1 ]
机构
[1] Stanford Univ, Sch Med, Beckman Ctr, Dept Mol & Cellular Physiol, Stanford, CA 94305 USA
关键词
D O I
10.1002/bies.10152
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Somatic or inherited mutations in the adenomatous polyposis coli (APC) gene are a frequent cause of colorectal cancer in humans. APC protein has an important tumor suppression function to reduce cellular levels of the signaling protein beta-catenin and, thereby, inhibit beta-catenin and T-cell-factor-mediated gene expression. In addition, APC protein binds to microtubules in vertebrate cells and localizes to actin-rich adherens junctions in epithelial cells of the fruit fly Drosophila (Fig. 1). Very little is known, however, about the function of these cytoskeletal associations. Recently, Hamada and Bienz have described a potential role for Drosophila E-APC in cellular adhesion,((1)) which offers new clues to APC function in embryonic development, and potentially colorectal adenoma formation and tumor progression in humans. (C) 2002 Wiley Periodicals, Inc.
引用
收藏
页码:771 / 774
页数:4
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