2011
Hepatocyte growth factor upregulation promotes carcinogenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via Akt and COX-2 pathways
Ogunwobi O, Liu C. Hepatocyte growth factor upregulation promotes carcinogenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via Akt and COX-2 pathways. Clinical & Experimental Metastasis 2011, 28: 721-731. PMID: 21744257, PMCID: PMC3732749, DOI: 10.1007/s10585-011-9404-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCadherinsCarcinoma, HepatocellularCell AdhesionCell DifferentiationCell Line, TumorCell MovementCell ProliferationCyclooxygenase 2Enzyme-Linked Immunosorbent AssayEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesHepatocyte Growth FactorLiver Neoplasms, ExperimentalMiceMice, Inbred BALB CNeoplasm InvasivenessPhosphorylationProto-Oncogene Proteins c-aktReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionUp-RegulationVimentinConceptsEpithelial-mesenchymal transitionHepatocyte growth factorCyclooxygenase-2Hepatocellular carcinomaBNL cellsMarkers of EMTDevelopment of HCCAdvanced hepatocellular carcinomaCOX-2 pathwayMetastatic hepatocellular carcinomaUpregulation of HGFMesenchymal characteristicsGrowth factor upregulationE-cadherinCharacteristic epithelial morphologyCancer mortalitySubsequent metastasisEMT markersImportant causeMigratory capacityHCC cellsBNL CLCancer progressionCollagen 1Growth factorDNA Methylation Suppresses Expression of the Urea Cycle Enzyme Carbamoyl Phosphate Synthetase 1 (CPS1) in Human Hepatocellular Carcinoma
Liu H, Dong H, Robertson K, Liu C. DNA Methylation Suppresses Expression of the Urea Cycle Enzyme Carbamoyl Phosphate Synthetase 1 (CPS1) in Human Hepatocellular Carcinoma. American Journal Of Pathology 2011, 178: 652-661. PMID: 21281797, PMCID: PMC3069978, DOI: 10.1016/j.ajpath.2010.10.023.Peer-Reviewed Original ResearchMeSH KeywordsCarbamoyl-Phosphate Synthase (Ammonia)Carcinoma, HepatocellularCell Line, TumorCpG IslandsDNA MethylationGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 3-betaHepatocytesHumansLiver NeoplasmsPromoter Regions, GeneticQuaternary Ammonium CompoundsRNA, MessengerUreaConceptsHCC cellsNoncancerous tissuesTumor tissueHepatocyte paraffin 1 antibodySurgical pathology practiceLiver cancer tissuesHuman HCC cellsCPS1 expressionHCC tumor tissuesLiver tumor tissuesHuman hepatocellular carcinomaHuman hepatocellular carcinoma cellsCultured human primary hepatocytesHuman primary hepatocytesHepatocellular carcinoma cellsHepatocellular carcinomaCPS1 geneRate-limiting enzymeLiver carcinogenesisCancer tissuesSynthetase 1Potential biomarkersCarbamoyl phosphate synthetase 1Pathology practiceCarcinoma cells
2004
STAT3 induces anti-hepatitis C viral activity in liver cells
Zhu H, Shang X, Terada N, Liu C. STAT3 induces anti-hepatitis C viral activity in liver cells. Biochemical And Biophysical Research Communications 2004, 324: 518-528. PMID: 15474458, DOI: 10.1016/j.bbrc.2004.09.081.Peer-Reviewed Original ResearchMeSH KeywordsAntiviral AgentsBlotting, NorthernBlotting, WesternCarcinoma, HepatocellularCell LineCell Line, TumorCytokinesDNA-Binding ProteinsDose-Response Relationship, DrugEnzyme InhibitorsGenes, DominantHepacivirusHumansInflammationInterferonsInterleukin-6LigandsLiverLiver NeoplasmsLuciferasesPlasmidsProtein Structure, TertiaryReverse Transcriptase Polymerase Chain ReactionRibavirinRNARNA, MessengerSTAT3 Transcription FactorTime FactorsTrans-ActivatorsTransfectionTyrphostinsConceptsAnti-HCV activityInterferon alphaSTAT3 activationHuman hepatoma cellsHepatitis C virus infectionHCV subgenomic RNA replicationMain therapeutic regimenC virus infectionChronic liver diseaseCytokines IL-6Replicon cell linesIntracellular antiviral stateCell linesHepatoma cellsLiver diseaseTherapeutic regimenActivation of STAT3IL-6Virus infectionEstrogen receptorIFN treatmentAntiviral genesAntiviral pathwaysAntiviral activityAntiviral state
2003
A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation
Hildebrandt G, Duffner U, Olkiewicz K, Corrion L, Willmarth N, Williams D, Clouthier S, Hogaboam C, Reddy P, Moore B, Kuziel W, Liu C, Yanik G, Cooke K. A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation. Blood 2003, 103: 2417-2426. PMID: 14615370, DOI: 10.1182/blood-2003-08-2708.Peer-Reviewed Original ResearchConceptsMonocyte chemoattractant protein-1Idiopathic pneumonia syndromeAllogeneic bone marrow transplantationBone marrow transplantationChemokine receptor 2CCR2/MCPAllo-BMTPneumonia syndromeMarrow transplantationBronchoalveolar lavage fluid cellularityExperimental Idiopathic Pneumonia SyndromeBAL fluid levelsMouse BMT modelSoluble p55 TNF receptorTime of diagnosisPreliminary clinical findingsChemoattractant protein-1P55 TNF receptorDonor leukocytesLung injuryMajor complicationsAllogeneic recipientsBAL fluidLethal complicationPulmonary expression