Abstract
GNAQ mutations are early and frequent events in the pathology of Uveal Melanoma. These mutations hyper-activate PLCb-PKC-ERK1/2 signaling resulting in PKC dependence. Targeting GNAQ mutant Uveal Melanoma Cells with the PKC inhibitor AEB071 (Sotrastaurin) leads to pathway modulation and growth inhibition. The Myristoylated Alanine-rich C-kinase Substrate (MARCKS) is directly phosphorylated by PKC and can be used as a readout for PKC activation.
Citation Information: Mol Cancer Ther 2013;12(11 Suppl):C149.
Citation Format: Rosemary Barrett, Ribo Guo, Jing Yuan, Vesselina Cooke, Anthony Vattay, Joshua Korn, Guiqing Liang, Xin Li, Ramu Thiruvamoor, Andrew Wylie, Anka Bric, Nicholas Keen, William Sellers. The PKC inhibitor Sotrastaurin selectively inhibits the growth of GNAQ mutant uveal melanoma. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr C149.