2016
ALDOA functions as an oncogene in the highly metastatic pancreatic cancer
Ji S, Zhang B, Liu J, Qin Y, Liang C, Shi S, Jin K, Liang D, Xu W, Xu H, Wang W, Wu C, Liu L, Liu C, Xu J, Ni Q, Yu X. ALDOA functions as an oncogene in the highly metastatic pancreatic cancer. Cancer Letters 2016, 374: 127-135. PMID: 26854714, DOI: 10.1016/j.canlet.2016.01.054.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorCadherinsCarcinoma, Pancreatic DuctalCell Line, TumorFructose-Bisphosphate AldolaseGlycolysisHeterograftsHigh-Throughput Screening AssaysHumansMaleMiceMice, NudeNeoplasm InvasivenessNeoplasm MetastasisOncogenesPancreatic NeoplasmsReactive Oxygen SpeciesSignal TransductionConceptsHigh-throughput screening analysisAldolase APancreatic cancerRegulation of c-MycTGF-bE-cadherinAnalyzed gene expression signaturesRegulation of glycolysisResistant to conventional treatmentPancreatic cancer cell line PANC-1Cancer metabolic changesPrognosis of pancreatic cancerTransforming growth factor-bSubgroup of patientsCell line PANC-1Metastasis of pancreatic cancer cellsPoor prognosis of pancreatic cancerExpression regulationGene expression signaturesPancreatic cancer tissue samplesPancreatic cancer cellsGlycolytic genesGrowth factor BE-cadherin expressionCancer tissue samples
2011
Reactive Oxygen Species Is Essential for Cycloheximide to Sensitize Lexatumumab-Induced Apoptosis in Hepatocellular Carcinoma Cells
Zhao X, Cao M, Liu J, Zhu H, Nelson D, Liu C. Reactive Oxygen Species Is Essential for Cycloheximide to Sensitize Lexatumumab-Induced Apoptosis in Hepatocellular Carcinoma Cells. PLOS ONE 2011, 6: e16966. PMID: 21347335, PMCID: PMC3037406, DOI: 10.1371/journal.pone.0016966.Peer-Reviewed Original ResearchAntibodies, MonoclonalApoptosisBcl-2 Homologous Antagonist-Killer ProteinBcl-2-Associated X ProteinCarcinoma, HepatocellularCaspasesCell Line, TumorCycloheximideDrug InteractionsGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansIntracellular SpaceLiver NeoplasmsReactive Oxygen SpeciesManipulating the Bioenergetics of Alloreactive T Cells Causes Their Selective Apoptosis and Arrests Graft-Versus-Host Disease
Gatza E, Wahl D, Opipari A, Sundberg T, Reddy P, Liu C, Glick G, Ferrara J. Manipulating the Bioenergetics of Alloreactive T Cells Causes Their Selective Apoptosis and Arrests Graft-Versus-Host Disease. Science Translational Medicine 2011, 3: 67ra8. PMID: 21270339, PMCID: PMC3364290, DOI: 10.1126/scitranslmed.3001975.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBenzodiazepinesBone Marrow CellsBone Marrow TransplantationFemaleGraft vs Host DiseaseIsoantigensLactatesLymphocyte ActivationMetabolomeMiceMice, Inbred BALB CMice, Inbred C57BLMitochondrial Proton-Translocating ATPasesOxidative PhosphorylationOxygen ConsumptionReactive Oxygen SpeciesT-LymphocytesConceptsAlloreactive T cellsT cellsHost diseaseBM transplantationAerobic glycolysisAdenosine triphosphateAccumulation of acylcarnitinesBone marrow cellsFatty acid oxidationGraft-VersusLymphocyte reconstitutionImmune activationBMT modelBM cellsImmune disordersHematopoietic engraftmentTherapeutic strategiesOxidative phosphorylationSmall molecule inhibitorsMarrow cellsSuperoxide productionSufficient adenosine triphosphateMitochondrial membrane potentialMetabolic adaptationAcid oxidation