Journal
CANCER CELL
Volume 25, Issue 6, Pages 822-830Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2014.04.017
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Funding
- NIH [EY022611, CA132809, EY024134]
- California Institute for Regenerative Medicine [RB2-01547]
- Research to Prevent Blindness
- 973 program, China [2014CB964900, 2013CB967500]
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Uveal melanoma (UM) is the most common cancer in adult eyes. Approximately 80% of UMs harbor somatic activating mutations in GNAQ or GNA11 (encoding Gq or G11, respectively). Herein, we show in both cell culture and human tumors that cancer-associated Gq/11 mutants activate YAP, a major effector of the Hippo tumor suppressor pathway that is also regulated by G protein-coupled receptor signaling. YAP mediates the oncogenic activity of mutant Gq/11 in UM development, and the YAP inhibitor verteporfin blocks tumor growth of UM cells containing Gq/11 mutations. This study reveals an essential role of the Hippo-YAP pathway in Gq/11-induced tumorigenesis and suggests YAP as a potential drug target for UM patients carrying mutations in GNAQ or GNA11.
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