2015
The cell cycle regulator 14-3-3σ opposes and reverses cancer metabolic reprogramming
Phan L, Chou PC, Velazquez-Torres G, Samudio I, Parreno K, Huang Y, Tseng C, Vu T, Gully C, Su CH, Wang E, Chen J, Choi HH, Fuentes-Mattei E, Shin JH, Shiang C, Grabiner B, Blonska M, Skerl S, Shao Y, Cody D, Delacerda J, Kingsley C, Webb D, Carlock C, Zhou Z, Hsieh YC, Lee J, Elliott A, Ramirez M, Bankson J, Hazle J, Wang Y, Li L, Weng S, Rizk N, Wen YY, Lin X, Wang H, Wang H, Zhang A, Xia X, Wu Y, Habra M, Yang W, Pusztai L, Yeung SC, Lee MH. The cell cycle regulator 14-3-3σ opposes and reverses cancer metabolic reprogramming. Nature Communications 2015, 6: 7530. PMID: 26179207, PMCID: PMC4507299, DOI: 10.1038/ncomms8530.Peer-Reviewed Original ResearchMeSH Keywords14-3-3 ProteinsAdultAgedAged, 80 and overBiomarkers, TumorBreast NeoplasmsCell Line, TumorDisease-Free SurvivalEnergy MetabolismExoribonucleasesFemaleGene Expression Regulation, NeoplasticGene Knockout TechniquesGlutamineGlycolysisHCT116 CellsHumansMiddle AgedOrganelle BiogenesisPrognosisProteolysisProto-Oncogene Proteins c-mycUbiquitinationYoung AdultConceptsCancer metabolic reprogrammingMetabolic reprogrammingRecurrence-free survival ratesMetabolic gene expressionBreast cancer patientsCellular energy metabolismHallmarks of cancerMajor metabolic processesTumor glucose uptakeExtensive reprogrammingMetabolic programsMitochondrial biogenesisGene expressionTumorigenic transformationCancer glycolysisMolecular mechanismsReprogrammingCancer patientsMetabolic processesMetabolic shift
2014
Metabolic isoenzyme shifts in cancer as potential novel therapeutic targets
Ononye SN, Shi W, Wali VB, Aktas B, Jiang T, Hatzis C, Pusztai L. Metabolic isoenzyme shifts in cancer as potential novel therapeutic targets. Breast Cancer Research And Treatment 2014, 148: 477-488. PMID: 25395317, DOI: 10.1007/s10549-014-3194-1.Peer-Reviewed Original ResearchConceptsIsoform-specific inhibitorsMetabolic isoenzymesCancer cellsNeoplastic transformationMetabolic enzyme expressionFunctional redundancyEnzymatic functionIsoenzyme diversityAdditional isoformsCancer metabolismMetabolic enzymesSingle isoformMetabolic pathwaysPotential novel therapeutic targetNovel therapeutic targetMetabolic precursorsEnzyme expressionNormal cellsNew therapeutic strategiesStages of developmentIsoformsTherapeutic targetExpressionIsoenzyme expressionTreatment of cancerMitochondrial dysfunction in some triple-negative breast cancer cell lines: role of mTOR pathway and therapeutic potential
Pelicano H, Zhang W, Liu J, Hammoudi N, Dai J, Xu RH, Pusztai L, Huang P. Mitochondrial dysfunction in some triple-negative breast cancer cell lines: role of mTOR pathway and therapeutic potential. Breast Cancer Research 2014, 16: 434. PMID: 25209360, PMCID: PMC4303115, DOI: 10.1186/s13058-014-0434-6.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateCell Line, TumorElectron Transport Chain Complex ProteinsEnergy MetabolismFemaleGlucoseGlutathioneHumansHydrocarbons, BrominatedLactic AcidMitochondriaNADPOxidation-ReductionOxygen ConsumptionPropionatesReactive Oxygen SpeciesReceptor, ErbB-2Receptors, EstrogenReceptors, ProgesteroneSignal TransductionTOR Serine-Threonine KinasesTriple Negative Breast NeoplasmsConceptsTNBC cellsBreast cancer cellsBreast cancerCancer cellsPositive cellsMetabolic alterationsIntroductionTriple-negative breast cancerMTOR pathwayEstrogen receptor-positive cellsER-positive cellsEffective therapeutic approachReceptor-positive cellsBreast cancer subtypesBreast cancer cell linesEffective therapeutic strategyTriple-negative breast cancer cell linesCurrent chemotherapeutic agentsMalignant breast cancerProfound metabolic alterationsHigher glucose uptakeInhibition of glycolysisCancer cell linesPoor prognosisLower mitochondrial respirationMitochondrial respiration