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Article: SIRT3 Opposes Reprogramming of Cancer Cell Metabolism through HIF1α Destabilization

TitleSIRT3 Opposes Reprogramming of Cancer Cell Metabolism through HIF1α Destabilization
Authors
Issue Date2011
PublisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/ccell
Citation
Cancer Cell, 2011, v. 19 n. 3, p. 416-428 How to Cite?
AbstractTumor cells exhibit aberrant metabolism characterized by high glycolysis even in the presence of oxygen. This metabolic reprogramming, known as the Warburg effect, provides tumor cells with the substrates required for biomass generation. Here, we show that the mitochondrial NAD-dependent deacetylase SIRT3 is a crucial regulator of the Warburg effect. Mechanistically, SIRT3 mediates metabolic reprogramming by destabilizing hypoxia-inducible factor-1α (HIF1α), a transcription factor that controls glycolytic gene expression. SIRT3 loss increases reactive oxygen species production, leading to HIF1α stabilization. SIRT3 expression is reduced in human breast cancers, and its loss correlates with the upregulation of HIF1α target genes. Finally, we find that SIRT3 overexpression represses glycolysis and proliferation in breast cancer cells, providing a metabolic mechanism for tumor suppression. © 2011 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/180746
ISSN
2015 Impact Factor: 23.214
2015 SCImago Journal Rankings: 13.922
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFinley, Len_US
dc.contributor.authorCarracedo, Aen_US
dc.contributor.authorLee, Jen_US
dc.contributor.authorSouza, Aen_US
dc.contributor.authorEgia, Aen_US
dc.contributor.authorZhang, Jen_US
dc.contributor.authorTeruyaFeldstein, Jen_US
dc.contributor.authorMoreira, Pen_US
dc.contributor.authorCardoso, Sen_US
dc.contributor.authorClish, Cen_US
dc.contributor.authorPandolfi, Pen_US
dc.contributor.authorHaigis, Men_US
dc.date.accessioned2013-01-28T01:42:13Z-
dc.date.available2013-01-28T01:42:13Z-
dc.date.issued2011en_US
dc.identifier.citationCancer Cell, 2011, v. 19 n. 3, p. 416-428en_US
dc.identifier.issn1535-6108en_US
dc.identifier.urihttp://hdl.handle.net/10722/180746-
dc.description.abstractTumor cells exhibit aberrant metabolism characterized by high glycolysis even in the presence of oxygen. This metabolic reprogramming, known as the Warburg effect, provides tumor cells with the substrates required for biomass generation. Here, we show that the mitochondrial NAD-dependent deacetylase SIRT3 is a crucial regulator of the Warburg effect. Mechanistically, SIRT3 mediates metabolic reprogramming by destabilizing hypoxia-inducible factor-1α (HIF1α), a transcription factor that controls glycolytic gene expression. SIRT3 loss increases reactive oxygen species production, leading to HIF1α stabilization. SIRT3 expression is reduced in human breast cancers, and its loss correlates with the upregulation of HIF1α target genes. Finally, we find that SIRT3 overexpression represses glycolysis and proliferation in breast cancer cells, providing a metabolic mechanism for tumor suppression. © 2011 Elsevier Inc.en_US
dc.languageengen_US
dc.publisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/ccellen_US
dc.relation.ispartofCancer Cellen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Hypoxiaen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshFibroblasts - Cytology - Metabolismen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshGlucose - Metabolismen_US
dc.subject.meshGlycolysisen_US
dc.subject.meshHek293 Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshHypoxia-Inducible Factor 1, Alpha Subunit - Metabolismen_US
dc.subject.meshImmunoblottingen_US
dc.subject.meshMaleen_US
dc.subject.meshMetabolomics - Methodsen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, 129 Strainen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshNeoplasms - Genetics - Metabolism - Pathologyen_US
dc.subject.meshProtein Stabilityen_US
dc.subject.meshReactive Oxygen Species - Metabolismen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshSirtuin 3 - Genetics - Metabolismen_US
dc.subject.meshTransplantation, Heterologousen_US
dc.titleSIRT3 Opposes Reprogramming of Cancer Cell Metabolism through HIF1α Destabilizationen_US
dc.typeArticleen_US
dc.identifier.emailZhang, J: jzhang1@hku.hken_US
dc.identifier.authorityZhang, J=rp01713en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.ccr.2011.02.014en_US
dc.identifier.pmid21397863-
dc.identifier.scopuseid_2-s2.0-79952501323en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79952501323&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume19en_US
dc.identifier.issue3en_US
dc.identifier.spage416en_US
dc.identifier.epage428en_US
dc.identifier.isiWOS:000288642500013-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFinley, L=26538558300en_US
dc.identifier.scopusauthoridCarracedo, A=8549430700en_US
dc.identifier.scopusauthoridLee, J=42761680100en_US
dc.identifier.scopusauthoridSouza, A=36017628400en_US
dc.identifier.scopusauthoridEgia, A=12647355200en_US
dc.identifier.scopusauthoridZhang, J=22137260600en_US
dc.identifier.scopusauthoridTeruyaFeldstein, J=7004187581en_US
dc.identifier.scopusauthoridMoreira, P=7006510583en_US
dc.identifier.scopusauthoridCardoso, S=7102228036en_US
dc.identifier.scopusauthoridClish, C=35460787900en_US
dc.identifier.scopusauthoridPandolfi, P=35070270200en_US
dc.identifier.scopusauthoridHaigis, M=6603254624en_US

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