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  current news   Press   selected story    
     
  23rd April  
 

A role for TAZ in migration, invasion, and tumorigenesis of breast cancer cells.

 
 




Authors
Siew Wee Chan, Chun Jye Lim, Ke Guo, Chee Peng Ng, Ian Lee, Walter Hunziker, Qi Zeng, and Wanjin Hong.

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

Correspondence should be addressed to Wanjin HONG: mcbhwj@imcb.a-star.edu.sg

Abstract
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 lowexpressing 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 f20% 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.

 
 


 
 

Figure & Legend: TAZ knockdown in MCF7 cells suppresses anchorage-independent growth in soft-agar. A, soft-agar growth of MCF7-control (upper panel) and MCF7-KD-652 (lower panel) cells was assessed and photographed. B, the appearance of live colonies in soft-agar of MCF7-control (left panel) and MCF7-KD-652 (right panel) cells was photographed at higher amplification.

Published in Cancer Research (2008) Apr 15, Vol. 68:8 Pp 2592-8

For more information on Wanjin HONG’s Lab, Please Click here.