title: What can humans learn from flies about adenomatous polyposis coli?
abstract: 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, which offers new clues to APC function in embryonic development, and potentially colorectal adenoma formation and tumor progression in humans.
authors.affiliation: Department of Molecular and Cellular Physiology, Stanford University School of Medicine, CA 94305-5435, USA. angelab@stanford.edu
authors.forename: Angela I M
authors.initials: AI
authors.lastname: Barth
authors.forename: W James
authors.initials: WJ
authors.lastname: Nelson
mesh_terms: D011125:Adenomatous Polyposis Coli / Q000235:genetics; D025601:Adenomatous Polyposis Coli Protein / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D002448:Cell Adhesion; D015179:Colorectal Neoplasms / Q000378:metabolism; D004330:Drosophila; D006801:Humans; D008954:Models, Biological; D009154:Mutation
chemical_list: D025601:Adenomatous Polyposis Coli Protein