2012
Cyclooxygenase‐2 and Akt mediate multiple growth‐factor‐induced epithelial‐mesenchymal transition in human hepatocellular carcinoma
Ogunwobi O, Wang T, Zhang L, Liu C. Cyclooxygenase‐2 and Akt mediate multiple growth‐factor‐induced epithelial‐mesenchymal transition in human hepatocellular carcinoma. Journal Of Gastroenterology And Hepatology 2012, 27: 566-578. PMID: 22097969, PMCID: PMC3288221, DOI: 10.1111/j.1440-1746.2011.06980.x.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminsAlpha 1-AntitrypsinAnimalsCadherinsCarcinoma, HepatocellularCell MovementCell TransplantationCollagen Type ICyclooxygenase 2DinoprostoneEpidermal Growth FactorEpithelial-Mesenchymal TransitionFibroblast Growth Factor 2FibronectinsGene ExpressionHepatocyte Growth FactorHumansMiceOncogene Protein v-aktRNA, Small InterferingSignal TransductionTransforming Growth Factor beta1Tumor Cells, CulturedVimentinConceptsEpithelial-mesenchymal transitionCyclooxygenase-2Hepatocellular carcinomaBasic fibroblast growth factorGrowth factorProstaglandin E2Metastatic hepatocellular carcinomaProgression of HCCEffective therapeutic strategyExpression of vimentinHepatocyte growth factorGrowth factor βHuman hepatocellular carcinomaFibroblast growth factorAssociated hepatitisChemopreventive strategiesEpidermal growth factorMultiple growth factorsTherapeutic strategiesMesenchymal changesSignificant mortalityAkt pathwayMolecular targetingCancer invasionAkt
2009
Hepatocellular Carcinoma Immunopathogenesis: Clinical Evidence for Global T Cell Defects and an Immunomodulatory Role for Soluble CD25 (sCD25)
Cabrera R, Ararat M, Cao M, Xu Y, Wasserfall C, Atkinson M, Liu C, Nelson D. Hepatocellular Carcinoma Immunopathogenesis: Clinical Evidence for Global T Cell Defects and an Immunomodulatory Role for Soluble CD25 (sCD25). Digestive Diseases And Sciences 2009, 55: 484-495. PMID: 19714465, PMCID: PMC3161029, DOI: 10.1007/s10620-009-0955-5.Peer-Reviewed Original ResearchConceptsT cell responsesHCC patientsHepatocellular carcinomaCell responsesTumor burdenImpaired T cell responsesLower IFN-γ productionEffector T cell responsesIL-2 receptor alpha chainATP production assaysLevels of sCD25Tolerogenic tumor environmentIFN-γ ELISPOTEffector T cellsT cell immunityT cell reactivityIFN-γ productionIL-2 supplementationT cell defectsDose-dependent mannerReceptor alpha chainIL-2 signalingSerum sCD25Soluble CD25Worse survival
2003
CD8+ T‐cell interaction with HCV replicon cells: Evidence for both cytokine‐ and cell‐mediated antiviral activity
Liu C, Zhu H, Tu Z, Xu Y, Nelson D. CD8+ T‐cell interaction with HCV replicon cells: Evidence for both cytokine‐ and cell‐mediated antiviral activity. Hepatology 2003, 37: 1335-1342. PMID: 12774012, DOI: 10.1053/jhep.2003.50207.Peer-Reviewed Original ResearchConceptsHepatitis C virusHCV replicon cellsAntiviral activityReplicon cellsHCV repliconMechanisms of HCVAnti-tumor necrosis factor alphaHCV subgenomic replicon systemAnti-interferon gammaDirect cytolytic effectHLA-A11 alleleNecrosis factor alphaHLA class IHost immune responseSubgenomic replicon systemT cell interactionsT-cell bindingHCV nonstructural proteinsCytolytic functionHCV interactionC virusSpecific lysisInfected hepatocytesTNF-alphaAntiviral effectGene expression associated with interferon alfa antiviral activity in an HCV replicon cell line
Zhu H, Zhao H, Collins C, Eckenrode S, Run Q, McIndoe R, Crawford J, Nelson D, She J, Liu C. Gene expression associated with interferon alfa antiviral activity in an HCV replicon cell line. Hepatology 2003, 37: 1180-1188. PMID: 12717400, DOI: 10.1053/jhep.2003.50184.Peer-Reviewed Original ResearchMeSH KeywordsAntiviral AgentsCarcinoma, HepatocellularDNA-Binding ProteinsGene ExpressionHepacivirusHepatitis C, ChronicHepatocytesHumansInterferon-alphaLiver NeoplasmsRNA, ViralSignal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorTrans-ActivatorsTumor Cells, CulturedViral ProteinsVirus ReplicationConceptsIFN-alpha antiviral activityIFN-alphaAntiviral activityReplicon cellsHCV replicon cell culture systemChronic hepatitis C viral infectionHepatitis C viral infectionHCV subgenomic RNA replicationHCV replicon cell linesC viral infectionOnly therapeutic optionDirect antiviral activityReplicon cell linesAnti-HCV activityHepatoma cellsDifferent gene expression profilesFeasible experimental modelIFN-alpha signalingCDNA microarray analysisGene expression profilesTherapeutic optionsActivation of STAT3Antiviral efficacyViral infectionResponsive genesInterleukin-1 Inhibits Hepatitis C Virus Subgenomic RNA Replication by Activation of Extracellular Regulated Kinase Pathway
Zhu H, Liu C. Interleukin-1 Inhibits Hepatitis C Virus Subgenomic RNA Replication by Activation of Extracellular Regulated Kinase Pathway. Journal Of Virology 2003, 77: 5493-5498. PMID: 12692250, PMCID: PMC153991, DOI: 10.1128/jvi.77.9.5493-5498.2003.Peer-Reviewed Original ResearchConceptsInterferon-stimulated genesHepatitis C virusInterleukin-1Antiviral activityHCV subgenomic RNA replicationDirect antiviral activityIL-1 productionReplicon cell linesNovel antiviral pathwayViral protein expressionViral clearanceC virusChronic infectionInflammatory processRNA replicationExtracellular-regulated kinase (ERK) pathwayAntiviral pathwaysInhibitory effectProtein expressionCell linesKinase pathwayKinase activationActivationPatientsInfection