{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sinik L"],"funding":["CCR NIH HHS","HHS | NIH | National Institute of Child Health and Human Development (NICHD)","Melanoma Research Alliance (MRA)","NICHD NIH HHS","NIDDK NIH HHS","Merck (Merck &amp; Co., Inc.)","NCI NIH HHS","HHS | NIH | National Cancer Institute (NCI)"],"pagination":["278-288"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9787186"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(2)"],"pubmed_abstract":["Molecularly-targeted agents have improved outcomes for a subset of patients with <i>BRAF</i>-mutated melanoma, but treatment of resistant and <i>BRAF</i> wild-type tumors remains a challenge. The MERTK receptor tyrosine kinase is aberrantly expressed in melanoma and can contribute to oncogenic phenotypes. Here we report the effect of treatment with a MERTK-selective small molecule inhibitor, UNC2025, in preclinical models of melanoma. In melanoma cell lines, treatment with UNC2025 potently inhibited phosphorylation of MERTK and downstream signaling, induced cell death, and decreased colony formation. In patient-derived melanoma xenograft models, treatment with UNC2025 blocked or significantly reduced tumor growth. Importantly, UNC2025 had similar biochemical and functional effects in both "],"journal":["Molecular cancer therapeutics"],"pubmed_title":["Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma."],"pmcid":["PMC9787186"],"funding_grant_id":["K12HD072245","P30 CA046934","K12 HD072245","HHSN261200800001E","P30 DK057516","HHSN261200800001C","Saban Family Foundation-MRA Team Science Award"],"pubmed_authors":["Carrico J","Kami R","Tentler JJ","Robinson WA","Eckhardt SG","Bagby SM","Sinik L","Graham DK","DeRyckere D","Wang X","Minson KA","Burstyn-Cohen T","Earp HS","Frye SV"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma.","description":"Molecularly-targeted agents have improved outcomes for a subset of patients with <i>BRAF</i>-mutated melanoma, but treatment of resistant and <i>BRAF</i> wild-type tumors remains a challenge. The MERTK receptor tyrosine kinase is aberrantly expressed in melanoma and can contribute to oncogenic phenotypes. Here we report the effect of treatment with a MERTK-selective small molecule inhibitor, UNC2025, in preclinical models of melanoma. In melanoma cell lines, treatment with UNC2025 potently inhibited phosphorylation of MERTK and downstream signaling, induced cell death, and decreased colony formation. In patient-derived melanoma xenograft models, treatment with UNC2025 blocked or significantly reduced tumor growth. Importantly, UNC2025 had similar biochemical and functional effects in both ","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Feb","modification":"2025-04-22T13:17:18.533Z","creation":"2025-04-06T00:39:37.224Z"},"accession":"S-EPMC9787186","cross_references":{"pubmed":["30482852"],"doi":["10.1158/1535-7163.mct-18-0456","10.1158/1535-7163.MCT-18-0456"]}}