This Article Full Text Full Text (PDF) Supplementary Data Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Chan, S. W. Articles by Hong, W. Search for Related Content PubMed PubMed Citation Articles by Chan, S. W. Articles by Hong, W.

A Role for TAZ in Migration, Invasion, and Tumorigenesis of Breast Cancer Cells

Cancer and Developmental Cell Biology Division, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore

Requests for reprints: Wanjin Hong, Institute of Molecular and Cell Biology, 61 Biopolis Drive, Singapore 138673, Singapore. Phone: 65-6586-9606; Fax: 65-6779-1117; E-mail: mcbhwj{at}imcb.a-star.edu.sg.

Key Words: TAZ • WWTR1 • breast cancer • cell migration • cell invasion • tumorigenesis

TAZ (WWTR1), identified as a 14-3-3 binding protein with a PDZ binding motif, modulates mesenchymal stem cell differentiation. We now show that TAZ plays a critical role in the migration, invasion, and tumorigenesis of breast cancer cells. TAZ is conspicuously expressed in human breast cancer cell lines in which its expression levels generally correlate with the invasiveness of cancer cells. Overexpression of TAZ in low-expressing MCF10A cells causes morphologic changes characteristic of cell transformation and promotes cell migration and invasion. Conversely, RNA interference–mediated knockdown of TAZ expression in MCF7 and Hs578T cells reduces cell migration and invasion. TAZ knockdown in MCF7 cells also retards anchorage-independent growth in soft agar and tumorigenesis in nude mice. Significantly, TAZ is overexpressed in 20% of breast cancer samples. These results indicate that TAZ plays a role in the migration, invasion, and tumorigenesis of breast cancer cells and thus presents a novel target for the detection and treatment of breast cancer. [Cancer Res 2008;68(8):2592–8]