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 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 approximately 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.
Highlights
Breast cancer is the leading type of cancer occurring in women and it is the second leading type of death-causing cancer in women in the United States [1]
The epithelial clusters of MCF7 cells became more densely packed with cells when TAZ expression was knocked down
It is conceivable that TAZ overexpression in breast cancer may trigger the loss of epithelial property to promote the migratory property, an important event for ductal carcinoma in situ to progress into IDC
Summary
Breast cancer is the leading type of cancer occurring in women and it is the second leading type of death-causing cancer in women in the United States [1]. Understanding the molecular mechanisms governing the initiation, progression, and metastasis of breast cancer is important for the prevention, detection, and treatment of this prevailing disease. A recent genomics study revealed that the gene for the tumor suppressor p53 is the most frequently mutated in breast cancers [2]. Breast cancers can be grouped into those positive for estrogen receptor-a (ER-a) and those negative for ER-a. ER-a–positive cancers can be effectively treated by inhibiting the function of ER-a because ER-a is important for the growth of these cells, whereas the growth of ER-a–negative cells is no longer dependent on ER-a. ER-a–negative breast cancers are resistant to ER-a–based treatments [3].
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