{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Suh J"],"funding":["Ministry of Trade, Industry and Energy","Ministry of Education","Institute for Basic Science","Korea Drug Development Fund","Korea Health Industry Development Institute","Ministry of Health and Welfare","Ministry of Science, ICT and Future Planning","National Research Foundation of Korea"],"pagination":["101342"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10829737"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5(1)"],"pubmed_abstract":["Chondrosarcomas represent the second most common primary bone malignancy. Despite the vulnerability of chondrosarcoma cells to nicotinamide adenine dinucleotide (NAD<sup>+</sup>) depletion, targeting the NAD<sup>+</sup> synthesis pathway remains challenging due to broad implications in biological processes. Here, we establish SIRT1 as a central mediator reinforcing the dependency of chondrosarcoma cells on NAD<sup>+</sup> metabolism via HIF-2α-mediated transcriptional reprogramming. SIRT1 knockdown abolishes aggressive phenotypes of chondrosarcomas in orthotopically transplanted tumors in mice. Chondrosarcoma cells thrive under glucose starvation by accumulating NAD<sup>+</sup> and subsequently activating the SIRT1-HIF-2α axis. Decoupling this link via SIRT1 inhibition unleashes apoptosis "],"journal":["Cell reports. Medicine"],"pubmed_title":["Decoupling NAD<sup>+</sup> metabolic dependency in chondrosarcoma by targeting the SIRT1-HIF-2α axis."],"pmcid":["PMC10829737"],"funding_grant_id":["IBS-R008-D1","RS-2023-00213119","NRF-2020R1A2C2012300","RS-2023-00217266","HI21C1218","NRF-2023R1A2C3003864","2021RIS-001","NRF-2020R1C1C1011369","NRF-2021R1I1A1A01059250"],"pubmed_authors":["Min J","Kim H","Yeon HJ","Kang HG","Kim YJ","Suh J","Wu MR","Hemberg M","Kim JH","Scimeca L"],"additional_accession":[]},"is_claimable":false,"name":"Decoupling NAD<sup>+</sup> metabolic dependency in chondrosarcoma by targeting the SIRT1-HIF-2α axis.","description":"Chondrosarcomas represent the second most common primary bone malignancy. Despite the vulnerability of chondrosarcoma cells to nicotinamide adenine dinucleotide (NAD<sup>+</sup>) depletion, targeting the NAD<sup>+</sup> synthesis pathway remains challenging due to broad implications in biological processes. Here, we establish SIRT1 as a central mediator reinforcing the dependency of chondrosarcoma cells on NAD<sup>+</sup> metabolism via HIF-2α-mediated transcriptional reprogramming. SIRT1 knockdown abolishes aggressive phenotypes of chondrosarcomas in orthotopically transplanted tumors in mice. Chondrosarcoma cells thrive under glucose starvation by accumulating NAD<sup>+</sup> and subsequently activating the SIRT1-HIF-2α axis. Decoupling this link via SIRT1 inhibition unleashes apoptosis ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jan","modification":"2026-07-15T04:38:40.47Z","creation":"2024-11-14T14:43:17.479Z"},"accession":"S-EPMC10829737","cross_references":{"pubmed":["38128534"],"doi":["10.1016/j.xcrm.2023.101342"]}}