{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lapadula D"],"funding":["NHLBI NIH HHS","NCI NIH HHS","NIH","NIGMS NIH HHS"],"pagination":["963-973"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6445713"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(4)"],"pubmed_abstract":["Uveal melanoma is the most common intraocular tumor in adults and often metastasizes to the liver, leaving patients with few options. Recurrent activating mutations in the G proteins, Gα<sub>q</sub> and Gα<sub>11</sub>, are observed in approximately 93% of all uveal melanomas. Although therapeutic intervention of downstream Gα<sub>q/11</sub> targets has been unsuccessful in treating uveal melanoma, we have found that the Gα<sub>q/11</sub> inhibitor, FR900359 (FR), effectively inhibits oncogenic Gα<sub>q/11</sub> signaling in uveal melanoma cells expressing either mutant Gα<sub>q</sub> or Gα<sub>11</sub>. Inhibition of oncogenic Gα<sub>q/11</sub> by FR results in cell-cycle arrest and induction of apoptosis. Furthermore, colony formation is prevented by FR treatment of uveal melanoma cells "],"journal":["Molecular cancer research : MCR"],"pubmed_title":["Effects of Oncogenic Gα<sub>q</sub> and Gα<sub>11</sub> Inhibition by FR900359 in Uveal Melanoma."],"pmcid":["PMC6445713"],"funding_grant_id":["P30CA056036","R01 CA218024","R01 GM088242","R01 GM056444","R03 CA202316","P30 CA056036","P01 HL114471","R01 GM56444","R01 CA109182","F31 CA225064","F31 CA224803"],"pubmed_authors":["McGrath D","Benovic JL","Randolph CE","Zhou N","Farias E","Tall GG","Aplin AE","Wedegaertner PB","Zhang L","Aguirre-Ghiso J","Terai M","Sato T","Lapadula D","Wu S","Purwin TJ","Charpentier TH"],"additional_accession":[]},"is_claimable":false,"name":"Effects of Oncogenic Gα<sub>q</sub> and Gα<sub>11</sub> Inhibition by FR900359 in Uveal Melanoma.","description":"Uveal melanoma is the most common intraocular tumor in adults and often metastasizes to the liver, leaving patients with few options. Recurrent activating mutations in the G proteins, Gα<sub>q</sub> and Gα<sub>11</sub>, are observed in approximately 93% of all uveal melanomas. Although therapeutic intervention of downstream Gα<sub>q/11</sub> targets has been unsuccessful in treating uveal melanoma, we have found that the Gα<sub>q/11</sub> inhibitor, FR900359 (FR), effectively inhibits oncogenic Gα<sub>q/11</sub> signaling in uveal melanoma cells expressing either mutant Gα<sub>q</sub> or Gα<sub>11</sub>. Inhibition of oncogenic Gα<sub>q/11</sub> by FR results in cell-cycle arrest and induction of apoptosis. Furthermore, colony formation is prevented by FR treatment of uveal melanoma cells ","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Apr","modification":"2026-03-15T21:01:52.747Z","creation":"2025-08-13T03:06:17.71Z"},"accession":"S-EPMC6445713","cross_references":{"pubmed":["30567972"],"doi":["10.1158/1541-7786.mcr-18-0574","10.1158/1541-7786.MCR-18-0574"]}}