2021
WEE1 inhibition induces anti-tumor immunity by activating ERV and the dsRNA pathway
Guo E, Xiao R, Wu Y, Lu F, Liu C, Yang B, Li X, Fu Y, Wang Z, Li Y, Huang Y, Li F, Wu X, You L, Qin T, Lu Y, Huang X, Ma D, Mills G, Sun C, Chen G. WEE1 inhibition induces anti-tumor immunity by activating ERV and the dsRNA pathway. Journal Of Experimental Medicine 2021, 219: e20210789. PMID: 34825915, PMCID: PMC8628262, DOI: 10.1084/jem.20210789.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsAntineoplastic Combined Chemotherapy ProtocolsCD8-Positive T-LymphocytesCell Cycle ProteinsCell Line, TumorEndogenous RetrovirusesEnzyme InhibitorsFemaleGene Expression Regulation, NeoplasticHCT116 CellsHumansImmune Checkpoint InhibitorsMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NODMice, SCIDNeoplasms, ExperimentalProtein-Tyrosine KinasesPyrazolesPyrimidinonesRNA, Double-StrandedSignal TransductionTumor BurdenConceptsImmune checkpoint blockadeAnti-tumor immunityEndogenous retroviral elementsWEE1 inhibitionCheckpoint blockadeCD8+ T cell-dependent mannerSensitivity to immune checkpoint blockadeResponse to immune checkpoint blockadeAnti-tumor T cellsCombination of WEE1 inhibitorT cell-dependent mannerPathway-targeted therapiesMultiple tumor modelsPopulation of patientsEmergence of resistanceDown-regulating FoxM1Viral defense pathwaysPD-L1Tumor regressionCombination therapyTargeted therapyCombination partnerT cellsPatient selectionWEE1 inhibitor
2016
Critical role of oncogenic KRAS in pancreatic cancer (Review)
LIU J, JI S, LIANG C, QIN Y, JIN K, LIANG D, XU W, SHI S, ZHANG B, LIU L, LIU C, XU J, NI Q, YU X. Critical role of oncogenic KRAS in pancreatic cancer (Review). Molecular Medicine Reports 2016, 13: 4943-4949. PMID: 27121414, DOI: 10.3892/mmr.2016.5196.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaPancreatic cancerGenetically engineered mouse modelsPancreatic intraepithelial neoplasiaDevelopment of pancreatic ductal adenocarcinomaFormation of pancreatic intraepithelial neoplasiaProgression of pancreatic ductal adenocarcinomaIntraepithelial neoplasiaHigher mortality rateMutated KRASDuctal adenocarcinomaMouse modelHuman malignanciesKRASKRAS signalingPharmacological inhibitionOncogenic KRASPharmacological targetsMortality rateCancerTargeting KRASMolecular mechanismsProgressionALDOA 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
2013
Phosphatidylinositol 3-Kinase–Independent Signaling Pathways Contribute to ICOS-Mediated T Cell Costimulation in Acute Graft-Versus-Host Disease in Mice
Li J, Heinrichs J, Leconte J, Haarberg K, Semple K, Liu C, Gigoux M, Kornete M, Piccirillo C, Suh W, Yu X. Phosphatidylinositol 3-Kinase–Independent Signaling Pathways Contribute to ICOS-Mediated T Cell Costimulation in Acute Graft-Versus-Host Disease in Mice. The Journal Of Immunology 2013, 191: 200-207. PMID: 23729441, PMCID: PMC4318500, DOI: 10.4049/jimmunol.1203485.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsDisease Models, AnimalGene Knock-In TechniquesGraft vs Host DiseaseInducible T-Cell Co-Stimulator ProteinLymphocyte ActivationMiceMice, 129 StrainMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicPhosphatidylinositol 3-KinaseSignal TransductionT-Lymphocyte SubsetsConceptsCD8 T cellsCD4 T cellsT cellsHost diseaseWild-type CD8 T cellsCD8 T cell compartmentAllogeneic bone marrow transplantationAcute Graft-VersusPathogenic potentialTotal T cellsAlloreactive T cellsBone marrow transplantationT cell compartmentWild-type T cellsIntracellular calcium mobilizationVivo pathogenic potentialT cell costimulationT cell activationKnockout T cellsAcute graftAcute GVHDGraft-VersusSevere GVHDGVHD modelMarrow transplantation
2012
Guardian and Selective Killer: The Versatile Functions of TLR3 in Hepatocellular Carcinoma
Liu C. Guardian and Selective Killer: The Versatile Functions of TLR3 in Hepatocellular Carcinoma. Journal Of The National Cancer Institute 2012, 104: 1780-1782. PMID: 23197496, PMCID: PMC3514168, DOI: 10.1093/jnci/djs475.Peer-Reviewed Original ResearchOPA1 downregulation is involved in sorafenib-induced apoptosis in hepatocellular carcinoma
Zhao X, Tian C, Puszyk W, Ogunwobi O, Cao M, Wang T, Cabrera R, Nelson D, Liu C. OPA1 downregulation is involved in sorafenib-induced apoptosis in hepatocellular carcinoma. Laboratory Investigation 2012, 93: 8-19. PMID: 23108376, PMCID: PMC3860369, DOI: 10.1038/labinvest.2012.144.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCarcinoma, HepatocellularCell Line, TumorCytochromes cDown-RegulationGene Knockdown TechniquesGTP PhosphohydrolasesHumansLiverLiver NeoplasmsMiceMice, SCIDMitochondriaNiacinamidePhenylurea CompoundsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRaf KinasesRas ProteinsRNA, Small InterferingSignal TransductionSorafenibXenograft Model Antitumor AssaysConceptsHepatocellular carcinomaSorafenib-induced apoptosisHCC xenograft tumor growthOptic atrophy 1HCC cellsPatients' hepatocellular carcinomaNon-tumor tissue samplesAdvanced hepatocellular carcinomaPathogenesis of HCCNovel therapeutic targetTumorigenesis of HCCXenograft tumor growthTumor tissue analysisNormal human primary hepatocytesHuman primary hepatocytesCell growth inhibitionSorafenib treatmentHCC patientsTherapeutic targetExposure of cellsTumor growthMitochondrial injuryPatientsSorafenibOPA1 expressionCyclooxygenase‐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
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 factorCharacterization of HCV Interactions with Toll-Like Receptors and RIG-I in Liver Cells
Eksioglu E, Zhu H, Bayouth L, Bess J, Liu H, Nelson D, Liu C. Characterization of HCV Interactions with Toll-Like Receptors and RIG-I in Liver Cells. PLOS ONE 2011, 6: e21186. PMID: 21695051, PMCID: PMC3117876, DOI: 10.1371/journal.pone.0021186.Peer-Reviewed Original ResearchMeSH KeywordsCell DeathCell Line, TumorDEAD Box Protein 58DEAD-box RNA HelicasesDown-RegulationHepacivirusHost-Pathogen InteractionsHumansInterferon-betaLiverProtein BindingReceptors, ImmunologicSignal TransductionTNF-Related Apoptosis-Inducing LigandToll-Like ReceptorsViral Envelope ProteinsVirus ReplicationConceptsHuh7.5 cellsViral replicationHCV chronic patientsExpression of TLR3Toll-like receptorsHCV envelope proteinsExpression levelsRIG-I expressionHCV interactionChronic patientsHCVTRAIL pathwayViral escapeViral infectionInnate immunityViral pathogenesisTLR3Induction of apoptosisAntiviral stateIFN inductionLow expression levelsLiver cellsLH86Envelope proteinIFNAbrogation of donor T-cell IL-21 signaling leads to tissue-specific modulation of immunity and separation of GVHD from GVL
Hanash A, Kappel L, Yim N, Nejat R, Goldberg G, Smith O, Rao U, Dykstra L, Na I, Holland A, Dudakov J, Liu C, Murphy G, Leonard W, Heller G, van den Brink M. Abrogation of donor T-cell IL-21 signaling leads to tissue-specific modulation of immunity and separation of GVHD from GVL. Blood 2011, 118: 446-455. PMID: 21596854, PMCID: PMC3138694, DOI: 10.1182/blood-2010-07-294785.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsGene Knockdown TechniquesGraft vs Host DiseaseGraft vs Leukemia EffectHumansImmunity, InnateInterleukin-21 Receptor alpha SubunitInterleukinsLymphocytes, Tumor-InfiltratingMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred DBAMice, KnockoutOrgan SpecificitySignal TransductionTissue DonorsT-LymphocytesTransplantation ImmunologyConceptsSeparation of GVHDDonor T cellsKO T cellsIL-21T cellsTissue-specific modulationGastrointestinal GVHDCytokine productionWild-type donor T cellsDonor regulatory T cellsTh cell cytokine productionPeripheral T cell functionMesenteric lymph nodesRegulatory T cellsTh cell functionIL-21 signalingInflammatory cytokine productionBM transplantation modelT cell functionLymphoma responseLymph nodesProinflammatory cytokinesTransplantation outcomesTransplantation modelGVHDIkaros-Notch axis in host hematopoietic cells regulates experimental graft-versus-host disease
Toubai T, Sun Y, Tawara I, Friedman A, Liu C, Evers R, Nieves E, Malter C, Chockley P, Maillard I, Winandy S, Reddy P. Ikaros-Notch axis in host hematopoietic cells regulates experimental graft-versus-host disease. Blood 2011, 118: 192-204. PMID: 21471527, PMCID: PMC3139384, DOI: 10.1182/blood-2010-12-324616.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen-Presenting CellsCD8-Positive T-LymphocytesCells, CulturedDendritic CellsDisease Models, AnimalFemaleGraft vs Host DiseaseHematopoiesisIkaros Transcription FactorImmunophenotypingMaleMiceMice, Inbred BALB CMice, Inbred C3HMice, Inbred C57BLMice, Mutant StrainsReceptor, Notch1Signal TransductionConceptsDendritic cellsAcute GVHDDonor T cell expansionExperimental bone marrow transplantationHost hematopoietic cellsInduction of GVHDAllogeneic T cellsBone marrow transplantationT cell expansionRelevant murine modelGvH responseAllostimulatory capacityHost diseaseWild-type controlsDC biologyMarrow transplantationPotent APCsActivation markersTLR stimulationT cellsMurine modelGVHDExperimental graftEnhanced stimulationIkaros deficiency
2005
Novel type I interferon IL-28A suppresses hepatitis C viral RNA replication
Zhu H, Butera M, Nelson D, Liu C. Novel type I interferon IL-28A suppresses hepatitis C viral RNA replication. Virology Journal 2005, 2: 80. PMID: 16146571, PMCID: PMC1232870, DOI: 10.1186/1743-422x-2-80.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntiviral AgentsBase SequenceCell LineGenes, MHC Class IHepacivirusHepatitis CHumansInterferon Regulatory Factor-1Interferon Type IInterferon-alphaInterferon-Stimulated Gene Factor 3Interleukin-10InterleukinsJanus KinasesMolecular Sequence DataRNA, ViralSignal TransductionSTAT Transcription FactorsVirus ReplicationConceptsInterferon-stimulated genesIL-28AAntiviral activityAntiviral efficacyHuman hepatoma cellsSide effectsChronic hepatitis C viral infectionHepatitis C viral infectionViral RNA replicationAntiviral response ratesHCV subgenomic RNA replicationIFNα-based therapyGenotype 1 infectionHCV chronic infectionC viral infectionIL-10 receptorIL-10 treatmentHLA class IType I IFNJAK-STATRNA replicationDose-dependent mannerHepatoma cellsExpression of ISGsUndesirable side effects
2004
Increasing T-cell age reduces effector activity but preserves proliferative capacity in a murine allogeneic major histocompatibility complex-mismatched bone marrow transplant model
Friedman J, Alpdogan O, van den Brink M, Liu C, Hurwitz D, Boyd A, Kupper T, Burakoff S. Increasing T-cell age reduces effector activity but preserves proliferative capacity in a murine allogeneic major histocompatibility complex-mismatched bone marrow transplant model. Transplantation And Cellular Therapy 2004, 10: 448-460. PMID: 15205666, DOI: 10.1016/j.bbmt.2004.03.005.Peer-Reviewed Original ResearchConceptsOld T cellsT cellsSurface antigen expressionCD8 cellsAntigen expressionEffector activityT cell receptor repertoireBone marrow transplant modelCD4 T cell expansionT-cell doseSeverity of GVHDType 1 cytokinesT cell expansionAntigen-driven proliferationT-cell groupAdult T-cellT-cell ageSuccinimidyl ester labelingYoung T cellsAge-dependent declineLethal GVHDHost diseasePathologic evidenceTransplant modelCytolytic function
2003
Gene 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 genes