Barth Angela I M, Nelson W James
Department of Molecular and Cellular Physiology, Stanford University School of Medicine, CA 94305-5435, USA.
Bioessays. 2002 Sep;24(9):771-4. doi: 10.1002/bies.10152.
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.
腺瘤性息肉病大肠杆菌(APC)基因的体细胞突变或遗传突变是人类结直肠癌的常见病因。APC蛋白具有重要的肿瘤抑制功能,可降低信号蛋白β-连环蛋白的细胞水平,从而抑制β-连环蛋白和T细胞因子介导的基因表达。此外,APC蛋白在脊椎动物细胞中与微管结合,并定位于果蝇上皮细胞中富含肌动蛋白的黏着连接(图1)。然而,对于这些细胞骨架关联的功能知之甚少。最近,滨田和比恩泽描述了果蝇E-APC在细胞黏附中的潜在作用,这为APC在胚胎发育中的功能以及人类结直肠腺瘤形成和肿瘤进展提供了新线索。