Mutant GNAQ promotes cell viability and migration of uveal melanoma cells through the activation of Notch signaling

摘要: The occurrence of guanine nucleotide binding protein (G protein), q polypeptide (GNAQ) mutations has been found to be high in the majority uveal melanomas. However, underlying molecular mechanism GNAQ modulating melanoma is poorly understood. aim present study was investigate role and mutant regulation cell viability migration cells. Uveal cells containing were transfected with scrambled or small-interfering RNA. Compared control, knockdown markedly inhibited migration. tumor without exhibited enhanced following transfection HA-GαqQL. Additionally, significantly downregulated expression Jag-1 (Notch ligand), Notch intracellular domain Hes-1 target gene) Conversely, overexpression promoted their expression. Cell induced by treatment 5 µmol/l MRK003, a signaling inhibitor. Furthermore, human influenza hemagglutinin A epitope (HA)-GαqQL into caused Yes-associated (YAP) dephosphorylation nuclear translocation, which stimulated Hes-1. Positive correlations observed between mRNA levels levels. no positive correlation YAP results suggested that mutation via activation, mediated translocation.