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
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
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 factor
2010
Inhibition of Neovascularization to Simultaneously Ameliorate Graft-vs-Host Disease and Decrease Tumor Growth
Penack O, Henke E, Suh D, King C, Smith O, Na I, Holland A, Ghosh A, Lu S, Jenq R, Liu C, Murphy G, Lu T, May C, Scheinberg D, Gao D, Mittal V, Heller G, Benezra R, van den Brink M. Inhibition of Neovascularization to Simultaneously Ameliorate Graft-vs-Host Disease and Decrease Tumor Growth. Journal Of The National Cancer Institute 2010, 102: 894-908. PMID: 20463307, PMCID: PMC2886094, DOI: 10.1093/jnci/djq172.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsAntibodies, MonoclonalAntigens, CDBone Marrow TransplantationCadherinsFemaleFlow CytometryFluorescent Antibody TechniqueGraft vs Host DiseaseHematopoietic Stem Cell TransplantationMiceMice, Inbred C57BLNeoplasmsNeovascularization, PathologicTransplantation, HomologousConceptsTumor growthAllo-BMTHost diseaseAllogeneic hematopoietic stem cell transplantationHematopoietic stem cell transplantationEndothelial cellsAllo-BMT recipientsGVHD target tissuesAllogeneic BM transplantationStem cell transplantationEndothelial progenitor cellsDecreases tumor growthInhibition of neovascularizationTumor-bearing miceTissue endothelial cellsAmeliorate graftDonor BMBM transplantationCell transplantationGVHDBone marrowTherapeutic targetingNeovascularizationOverall outcomeTumor vasculature