Jong Woo Lee, PhD
Research Scientist, Internal Medicine (Medical Oncology)Cards
About
Research
Publications
2020
E2F8 Induces Cell Proliferation and Invasion through the Epithelial–Mesenchymal Transition and Notch Signaling Pathways in Ovarian Cancer
Eoh KJ, Kim HJ, Lee JW, Kim LK, Park SA, Kim HS, Kim YT, Koo PJ. E2F8 Induces Cell Proliferation and Invasion through the Epithelial–Mesenchymal Transition and Notch Signaling Pathways in Ovarian Cancer. International Journal Of Molecular Sciences 2020, 21: 5813. PMID: 32823614, PMCID: PMC7460858, DOI: 10.3390/ijms21165813.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Knockdown TechniquesHumansMice, NudeMultivariate AnalysisNeoplasm InvasivenessOvarian NeoplasmsPrognosisProgression-Free SurvivalReceptors, NotchRepressor ProteinsSignal TransductionTumor BurdenXenograft Model Antitumor AssaysConceptsOvarian cancer cell linesProgression-free survivalOvarian cancer patientsOvarian cancerCancer cell linesCancer patientsCell proliferationCell linesKnockdown inhibited cell proliferationOvarian cancer tissuesNormal ovarian tissuesReduced tumor sizeOvarian cancer progressionPathway-related markersXenograft mouse modelEpithelial-mesenchymal transitionInhibited cell proliferationNotch signaling pathwayBio-functional effectsOvarian malignancyInduces cell proliferationTumor sizePrognostic markerClinical dataMouse modelSynthetic Lethal Targeting of Mitotic Checkpoints in HPV-Negative Head and Neck Cancer
Deneka AY, Einarson MB, Bennett J, Nikonova AS, Elmekawy M, Zhou Y, Lee JW, Burtness BA, Golemis EA. Synthetic Lethal Targeting of Mitotic Checkpoints in HPV-Negative Head and Neck Cancer. Cancers 2020, 12: 306. PMID: 32012873, PMCID: PMC7072436, DOI: 10.3390/cancers12020306.Peer-Reviewed Original ResearchG1/S checkpointNeck squamous cell carcinomaSingle-agent activitySquamous cell carcinomaHPV-negative headHPV-negative HNSCCHNSCC cell linesWEE1 inhibitor AZD1775S checkpointNegative HNSCCCell carcinomaHuman papillomavirusHNSCC cancerNeck cancerWorse outcomesSubset of drugsCommon mutational eventsDNA damageAnchorage-independent growthDual inhibitionClonogenic capacityClinical agentsSynthetic lethal targetingReduced activationHNSCC
2019
Combined Aurora Kinase A (AURKA) and WEE1 Inhibition Demonstrates Synergistic Antitumor Effect in Squamous Cell Carcinoma of the Head and Neck
Lee JW, Parameswaran J, Sandoval-Schaefer T, Eoh KJ, Yang DH, Zhu F, Mehra R, Sharma R, Gaffney SG, Perry EB, Townsend JP, Serebriiskii IG, Golemis EA, Issaeva N, Yarbrough WG, Koo JS, Burtness B. Combined Aurora Kinase A (AURKA) and WEE1 Inhibition Demonstrates Synergistic Antitumor Effect in Squamous Cell Carcinoma of the Head and Neck. Clinical Cancer Research 2019, 25: 3430-3442. PMID: 30755439, PMCID: PMC6548643, DOI: 10.1158/1078-0432.ccr-18-0440.Peer-Reviewed Original ResearchAnimalsAntineoplastic AgentsApoptosisAurora Kinase ACell Cycle ProteinsCell Line, TumorDisease Models, AnimalDrug SynergismFemaleFluorescent Antibody TechniqueGene ExpressionHumansMaleMiceNeoplasm GradingNeoplasm StagingProtein Kinase InhibitorsProtein-Tyrosine KinasesSquamous Cell Carcinoma of Head and NeckXenograft Model Antitumor AssaysThe Combination of MEK Inhibitor With Immunomodulatory Antibodies Targeting Programmed Death 1 and Programmed Death Ligand 1 Results in Prolonged Survival in Kras/p53-Driven Lung Cancer
Lee JW, Zhang Y, Eoh KJ, Sharma R, Sanmamed MF, Wu J, Choi J, Park HS, Iwasaki A, Kaftan E, Chen L, Papadimitrakopoulou V, Herbst RS, Koo JS. The Combination of MEK Inhibitor With Immunomodulatory Antibodies Targeting Programmed Death 1 and Programmed Death Ligand 1 Results in Prolonged Survival in Kras/p53-Driven Lung Cancer. Journal Of Thoracic Oncology 2019, 14: 1046-1060. PMID: 30771521, PMCID: PMC6542636, DOI: 10.1016/j.jtho.2019.02.004.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAnimalsAntineoplastic Agents, ImmunologicalAntineoplastic Combined Chemotherapy ProtocolsB7-H1 AntigenDrug SynergismFemaleLung NeoplasmsMAP Kinase Kinase KinasesMiceMice, KnockoutMice, TransgenicMyeloid-Derived Suppressor CellsProgrammed Cell Death 1 ReceptorProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)PyridonesPyrimidinonesSurvival AnalysisTumor Suppressor Protein p53ConceptsImmune cell populationsLung tumorsMEK inhibitorsDeath-1Survival outcomesLung cancerL1 mAbsTumor-infiltrating immune cell populationsTumor-infiltrating immune cellsCell death ligand 1Flow cytometryLung cancer mouse modelAdenoviral Cre recombinaseAutochthonous lung tumorsImmunomodulatory monoclonal antibodiesTumor-infiltrating CD8PD-L1 expressionSingle-agent therapyTumor-bearing lungsDeath ligand 1Tumor-free miceLung cancer modelCombinatorial antitumor effectCancer mouse modelCell populations
2017
Combinatorial Screening of Pancreatic Adenocarcinoma Reveals Sensitivity to Drug Combinations Including Bromodomain Inhibitor Plus Neddylation Inhibitor
Langdon CG, Platt JT, Means RE, Iyidogan P, Mamillapalli R, Klein M, Held MA, Lee JW, Koo JS, Hatzis C, Hochster HS, Stern DF. Combinatorial Screening of Pancreatic Adenocarcinoma Reveals Sensitivity to Drug Combinations Including Bromodomain Inhibitor Plus Neddylation Inhibitor. Molecular Cancer Therapeutics 2017, 16: 1041-1053. PMID: 28292938, PMCID: PMC5457712, DOI: 10.1158/1535-7163.mct-16-0794.Peer-Reviewed Original ResearchAdenosine TriphosphateAnimalsAntineoplastic AgentsApoptosisCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationDNA DamageDose-Response Relationship, DrugDrug CombinationsDrug Screening Assays, AntitumorDrug SynergismHigh-Throughput Nucleotide SequencingHumansMiceMitochondriaMolecular Targeted TherapyNeoplastic Stem CellsPancreatic NeoplasmsSuperoxidesXenograft Model Antitumor Assays
2016
GSK-3α Is a Novel Target of CREB and CREB-GSK-3α Signaling Participates in Cell Viability in Lung Cancer
Park SA, Lee JW, Herbst RS, Koo JS. GSK-3α Is a Novel Target of CREB and CREB-GSK-3α Signaling Participates in Cell Viability in Lung Cancer. PLOS ONE 2016, 11: e0153075. PMID: 27049759, PMCID: PMC4822949, DOI: 10.1371/journal.pone.0153075.Peer-Reviewed Original Research
2015
E2F8 as a Novel Therapeutic Target for Lung Cancer
Park SA, Platt J, Lee JW, López-Giráldez F, Herbst RS, Koo JS. E2F8 as a Novel Therapeutic Target for Lung Cancer. Journal Of The National Cancer Institute 2015, 107: djv151. PMID: 26089541, PMCID: PMC4651101, DOI: 10.1093/jnci/djv151.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCCAAT-Enhancer-Binding ProteinsCell Line, TumorCell ProliferationCell SurvivalChromatin ImmunoprecipitationFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticHumansImmunoblottingKaplan-Meier EstimateLung NeoplasmsMiceMolecular Targeted TherapyNeoplastic Stem CellsPromoter Regions, GeneticRepressor ProteinsTissue Array AnalysisUbiquitin-Protein LigasesUp-RegulationXenograft Model Antitumor AssaysConceptsTarget genesCell cycle regulationNovel therapeutic targetPromoter activity assaysCell proliferationCancer cellsExpression of UHRF1Transcription activatorAntisense morpholinoChromatin immunoprecipitationCycle regulationTherapeutic targetEmbryonic developmentE2F membersHuman lung cancer cellsMicroarray analysisInvasion analysisLung cancer cellsDirect bindingTumor growthE2F8Activity assaysPublic databasesColony formationUHRF1A Novel Small-Molecule Inhibitor Targeting CREB-CBP Complex Possesses Anti-Cancer Effects along with Cell Cycle Regulation, Autophagy Suppression and Endoplasmic Reticulum Stress
Lee JW, Park HS, Park SA, Ryu SH, Meng W, Jürgensmeier JM, Kurie JM, Hong WK, Boyer JL, Herbst RS, Koo JS. A Novel Small-Molecule Inhibitor Targeting CREB-CBP Complex Possesses Anti-Cancer Effects along with Cell Cycle Regulation, Autophagy Suppression and Endoplasmic Reticulum Stress. PLOS ONE 2015, 10: e0122628. PMID: 25897662, PMCID: PMC4405579, DOI: 10.1371/journal.pone.0122628.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdenocarcinoma of LungAnilidesAntineoplastic AgentsApoptosis Regulatory ProteinsAutophagyAutophagy-Related Protein 7Bcl-2-Like Protein 11Cell Cycle CheckpointsCell Line, TumorCyclic AMP Response Element-Binding ProteinDrug Screening Assays, AntitumorEndoplasmic Reticulum StressHumansInhibitory Concentration 50Kaplan-Meier EstimateLung NeoplasmsMembrane ProteinsMolecular Docking SimulationOrganophosphatesPeptide FragmentsProportional Hazards ModelsProtein BindingProto-Oncogene ProteinsSialoglycoproteinsUbiquitin-Activating EnzymesConceptsLung cancerHuman lung cancer cell linesEndoplasmic reticulum (ER) stress markersLung cancer cell linesNovel therapeutic strategiesPotential therapeutic targetAnti-cancer effectsNovel small molecule inhibitorPotential therapeutic agentCyclic AMP response element binding proteinAccumulation of p62Response element-binding proteinEndoplasmic reticulum stressCancer cell linesCancer deathCommon subtypeCell cycle arrestLung adenocarcinomaNew therapiesTherapeutic strategiesSmall molecule inhibitorsTherapeutic targetElement-binding proteinStress markersTherapeutic agents
2013
Hepatic SIRT1 Attenuates Hepatic Steatosis and Controls Energy Balance in Mice by Inducing Fibroblast Growth Factor 21
Li Y, Wong K, Giles A, Jiang J, Lee J, Adams A, Kharitonenkov A, Yang Q, Gao B, Guarente L, Zang M. Hepatic SIRT1 Attenuates Hepatic Steatosis and Controls Energy Balance in Mice by Inducing Fibroblast Growth Factor 21. Gastroenterology 2013, 146: 539-549.e7. PMID: 24184811, PMCID: PMC4228483, DOI: 10.1053/j.gastro.2013.10.059.Peer-Reviewed Original ResearchConceptsControl miceLivers of control miceFibroblast growth factor 21White adipose tissueHepatic overexpressionCirculating LevelsExpression of genesHepatic steatosisEnergy expenditureHormone-like regulatorsLKO miceFasted control miceHepatic expressionAbstractText Label="Background &Late-onset obesityAdipose tissueWild-type littermatesFatty acid oxidationNormal chow dietReal-time polymerase chain reaction assayControl energy balanceHormone fibroblast growth factor 21Severe hepatic steatosisFasting-induced steatosisLevels of FGF21
2011
Hepatic overexpression of SIRT1 in mice attenuates endoplasmic reticulum stress and insulin resistance in the liver
Li Y, Xu S, Giles A, Nakamura K, Lee J, Hou X, Donmez G, Li J, Luo Z, Walsh K, Guarente L, Zang M. Hepatic overexpression of SIRT1 in mice attenuates endoplasmic reticulum stress and insulin resistance in the liver. The FASEB Journal 2011, 25: 1664-1679. PMID: 21321189, PMCID: PMC3079300, DOI: 10.1096/fj.10-173492.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPGlucose Tolerance TestHep G2 CellsHumansImmunoblottingImmunohistochemistryInsulin ResistanceLiverMaleMiceMice, Inbred C57BLMice, KnockoutMice, ObeseObesityReceptors, LDLReverse Transcriptase Polymerase Chain ReactionSirtuin 1Unfolded Protein ResponseConceptsMammalian target of rapamycin complex 1Unfolded protein responseAdenovirus-mediated overexpressionOverexpression of SIRT1Endoplasmic reticulumSplicing of X-box binding protein 1Unfolded protein response signalingX-box binding protein 1Hepatic overexpressionInhibition of mammalian target of rapamycin complex 1Target of rapamycin complex 1Mammalian target of rapamycin complex 1 activityInsulin receptor signalingMouse embryonic fibroblastsRapamycin complex 1Endoplasmic reticulum stressBinding protein 1ER homeostasisExpression of GRP78Pathophysiology of human type 2 diabetesMammalian targetHuman type 2 diabetesProtein responseER stressInsulin resistance
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