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Up-regulation of C-Terminal Tensin-like Molecule Promotes the Tumorigenicity of Colon Cancer through β-Catenin

Center for Tissue Regeneration and Repair, Department of Biochemistry and Molecular Medicine, University of California-Davis, Sacramento, California

Requests for reprints: Su Hao Lo, Department of Biochemistry and Molecular Medicine, University of California-Davis, 4635 Second Avenue, Room 2000, Sacramento, CA 95817. Phone: 916-734-3656; Fax: 916-734-5750; E-mail: shlo{at}ucdavis.edu.

Key Words: cten • tensin • β-catenin • Wnt • colon cancer

C-terminal tensin-like (cten) is a focal adhesion molecule belonging to the tensin family. Previous studies have suggested that cten may function as a prostate-specific tumor suppressor. Here, we show that although cten is expressed at a very low level in normal colon, its expression is significantly up-regulated in colon cancer. Furthermore, a high population of cten is found in the nucleus, where it interacts with β-catenin, a critical player in the canonical Wnt pathway. This interaction may contribute to the role of cten in enhancing the colony formation, anchorage-independent growth, and invasiveness of colon cancer cells. Our studies have identified cten as a novel nuclear partner of β-catenin, showed an oncogenic activity of cten in colon cancers, and revealed cten as a potential biomarker and target for colon cancers. [Cancer Res 2009;69(11):4563–6]