{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gambi G"],"funding":["Amanda and Jonathan Eilian young investigator award","Amanda and Jonathan Eilian  young investigator award","Agence Nationale de la Recherche (ANR)","European Proteomics Infrastructure Consortium providing access (EPIC-XS)","Melanoma Research Alliance (MRA)","Agence Nationale de la Recherche","Belgian federation for cancer","European Proteomics Infrastructure Consortium providing access","Melanoma Research Alliance","ITMO Cancer","Ligue Nationale Contre le Cancer"],"pagination":["4555-4570"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9755964"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["82(24)"],"pubmed_abstract":["Tumor heterogeneity is a key feature of melanomas that hinders development of effective treatments. Aiming to overcome this, we identified LINC00518 (LENOX; lincRNA-enhancer of oxidative phosphorylation) as a melanoma-specific lncRNA expressed in all known melanoma cell states and essential for melanoma survival in vitro and in vivo. Mechanistically, LENOX promoted association of the RAP2C GTPase with mitochondrial fission regulator DRP1, increasing DRP1 S637 phosphorylation, mitochondrial fusion, and oxidative phosphorylation. LENOX expression was upregulated following treatment with MAPK inhibitors, facilitating a metabolic switch from glycolysis to oxidative phosphorylation and conferring resistance to MAPK inhibition. Consequently, combined silencing of LENOX and RAP2C synergized with "],"journal":["Cancer research"],"pubmed_title":["The LncRNA LENOX Interacts with RAP2C to Regulate Metabolism and Promote Resistance to MAPK Inhibition in Melanoma."],"pmcid":["PMC9755964"],"funding_grant_id":["N/A","ANR-10-IDEX-0002-02","ANR-10-LABX-0030","823839","FAF-F/2018/1184"],"pubmed_authors":["Mengus G","Davidson I","Davidson G","Demesmaeker E","Katopodi V","Leucci E","Cuomo A","Malouf GG","Bonaldi T","Gambi G"],"additional_accession":[]},"is_claimable":false,"name":"The LncRNA LENOX Interacts with RAP2C to Regulate Metabolism and Promote Resistance to MAPK Inhibition in Melanoma.","description":"Tumor heterogeneity is a key feature of melanomas that hinders development of effective treatments. Aiming to overcome this, we identified LINC00518 (LENOX; lincRNA-enhancer of oxidative phosphorylation) as a melanoma-specific lncRNA expressed in all known melanoma cell states and essential for melanoma survival in vitro and in vivo. Mechanistically, LENOX promoted association of the RAP2C GTPase with mitochondrial fission regulator DRP1, increasing DRP1 S637 phosphorylation, mitochondrial fusion, and oxidative phosphorylation. LENOX expression was upregulated following treatment with MAPK inhibitors, facilitating a metabolic switch from glycolysis to oxidative phosphorylation and conferring resistance to MAPK inhibition. Consequently, combined silencing of LENOX and RAP2C synergized with ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2025-04-22T04:32:35.841Z","creation":"2025-04-05T21:01:00.794Z"},"accession":"S-EPMC9755964","cross_references":{"pubmed":["36214632"],"doi":["10.1158/0008-5472.CAN-22-0959"]}}