Cell Motility Control in Human Colon Carcinoma

nloaded or invasion and metastasis are major obstacles to clinical treatment that rely on cell migration. Here, cidate a mechanism of colon carcinoma cell migration that is supported by the cell surface tetraspanin (tspan8), which is known to favor tumor progression and metastasis. This mechanism is unmasked by ng of E-cadherin or its associated adapter molecule p120-catenin (p120ctn), and it involves a switch in ng between the collagen-binding integrins α1β1 and α2β1. Direct interaction between E-cadherin and was documented by chemical cross-linking and immunohistologic analysis of colon carcinomas. High sion of Co-029 and cytoplasmic delocalization of p120ctn were each associated with poor prognosis. otility was reduced severely by antibody-mediated disruption of Co-029 only when p120ctn was silenced, ting that tumor progression may be hindered by Co-029 targeting. Our findings define a function for sugges tetraspanin Co-029 as a modifier of cancer cell motility and reveal an adhesion signaling network implicated in progression and metastasis. Cancer Res; 70(19); 7674–83. ©2010 AACR.