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Yu, Fa-Xing; Luo, Jing; Mo, Jung-Soon; Liu, Guangbo; Kim, Young Chul; Meng, Zhipeng; Zhao, Ling; Peyman, Gholam; Ouyang, Hong; Jiang, Wei; Zhao, Jiagang; Chen, Xu; Zhang, Liangfang; Wang, Cun-Yu; Bastian, Boris C.; Zhang, Kang; Guan, Kun-Liang
Cancer cell, 06/2014, Letnik: 25, Številka: 6Journal Article
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. Display omitted •Uveal melanoma-associated mutant Gq/11 activates YAP•YAP activation correlates with mutations of Gq/11 in uveal melanomas•YAP is essential for mutant Gq/11-induced uveal melanoma growth•YAP inhibitor suppresses mutant Gq/11-induced uveal melanoma development Yu et al. show that uveal melanomas with GNAQ- or GNA11-activating mutations have constitutively active YAP. These tumors, but not those driven by mutant BRAF, can be suppressed by YAP inhibition, suggesting YAP as a potential therapeutic target in these tumors.
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Dostop do baze podatkov JCR je dovoljen samo uporabnikom iz Slovenije. Vaš trenutni IP-naslov ni na seznamu dovoljenih za dostop, zato je potrebna avtentikacija z ustreznim računom AAI.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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