2021
Noncanonical open reading frames encode functional proteins essential for cancer cell survival
Prensner J, Enache O, Luria V, Krug K, Clauser K, Dempster J, Karger A, Wang L, Stumbraite K, Wang V, Botta G, Lyons N, Goodale A, Kalani Z, Fritchman B, Brown A, Alan D, Green T, Yang X, Jaffe J, Roth J, Piccioni F, Kirschner M, Ji Z, Root D, Golub T. Noncanonical open reading frames encode functional proteins essential for cancer cell survival. Nature Biotechnology 2021, 39: 697-704. PMID: 33510483, PMCID: PMC8195866, DOI: 10.1038/s41587-020-00806-2.Peer-Reviewed Original ResearchConceptsCancer cell linesOpen reading framePotential therapeutic targetCell linesGrowth inhibitory effectsCancer cell survivalInduced gene expression changesBreast cancerTherapeutic targetHuman cancer cell linesReading frameProtein expressionActive proteinProtein 1Gene expression changesCell survivalBiological effectsExpression changesViability defectsHuman genomeGenomic analysisCodon mutagenesisEctopic expressionFunctional proteinsKnockout
2018
Small molecule activators of protein phosphatase 2A for the treatment of castration-resistant prostate cancer.
McClinch K, Avelar R, Callejas D, Izadmehr S, Wiredja D, Perl A, Sangodkar J, Kastrinsky D, Schlatzer D, Cooper M, Kiselar J, Stachnik A, Yao S, Hoon D, McQuaid D, Zaware N, Gong Y, Brautigan D, Plymate S, Sprenger C, Oh W, Levine A, Kirschenbaum A, Sfakianos J, Sears R, DiFeo A, Ioannou Y, Ohlmeyer M, Narla G, Galsky M. Small molecule activators of protein phosphatase 2A for the treatment of castration-resistant prostate cancer. Cancer Research 2018, 78: canres.0123.2017. PMID: 29358171, PMCID: PMC5899650, DOI: 10.1158/0008-5472.can-17-0123.Peer-Reviewed Original ResearchConceptsCastrate-resistant prostate cancerAndrogen receptorProstate cancerCRPC cellsHuman castrate-resistant prostate cancerMultiple oncogenic signaling pathwaysSmall molecule activatorsAndrogen deprivation therapyAdvanced prostate cancerPrimary prostate cancerMurine xenograft modelGrowth inhibitory effectsDeprivation therapyCRPC treatmentTime-dependent mannerOncogenic signaling pathwaysPreclinical proofXenograft modelAR degradationCancer ResTumor suppressor PP2ATumor formationCancerAberrant reactivationSignaling pathways
2013
Piperine inhibits the proliferation of human prostate cancer cells via induction of cell cycle arrest and autophagy
Ouyang DY, Zeng LH, Pan H, Xu LH, Wang Y, Liu KP, He XH. Piperine inhibits the proliferation of human prostate cancer cells via induction of cell cycle arrest and autophagy. Food And Chemical Toxicology 2013, 60: 424-430. PMID: 23939040, DOI: 10.1016/j.fct.2013.08.007.Peer-Reviewed Original ResearchMeSH KeywordsAlkaloidsAutophagyBenzodioxolesCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalCyclin A1Cyclin D1Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Dose-Response Relationship, DrugDown-RegulationG1 PhaseHumansMalePiperidinesPolyunsaturated AlkamidesProstatic NeoplasmsUp-RegulationConceptsHuman prostate cancer cellsCell cycle arrestProstate cancer cellsPC-3 cellsPiperine treatmentCycle arrestCancer cellsHuman prostate cancer DU145Dose-dependent inhibitionCell linesAnti-proliferative effectsRobust cell cycle arrestGrowth inhibitory effectsLC3B puncta formationProstate cancer DU145LC3-II accumulationLNCaP cellsPresence of chloroquineCyclin D1LC3B-IILC3B punctaAntitumor mechanismAutophagy inhibitorInhibitory effectAntitumor activity
2012
An in vivo model of epithelial to mesenchymal transition reveals a mitogenic switch
Jahn SC, Law ME, Corsino PE, Parker NN, Pham K, Davis BJ, Lu J, Law BK. An in vivo model of epithelial to mesenchymal transition reveals a mitogenic switch. Cancer Letters 2012, 326: 183-190. PMID: 22906417, PMCID: PMC3705571, DOI: 10.1016/j.canlet.2012.08.013.Peer-Reviewed Original ResearchConceptsCancer cellsPre-EMT cellsNumber of genesMesenchymal transitionDNA microarray analysisEpithelial cell transitionPost-EMT cellsMitogenic signalingMicroarray analysisCell transitionMesenchymal phenotypeBreast cancer cellsERK phosphorylationLPA receptorsVivo modelMEK inhibitorsTissue architectureGrowth inhibitory effectsEpithelial cellsC-MetInhibitors/antagonistsPDGFCellsPhenotypeEMT
2009
The HDAC Inhibitor TSA Inhibits Cell Proliferation, Induces Apoptosis and Down-Regulates HER2 Protein and Gene Expression as a Single Agent and in Combination with Trastuzumab in Trastuzumab-Sensitive and -Resistant Breast Cancer Cell Lines.
Radke S, Perincheri S, Schulz V, Lerner B, Kumar A, Chandrasekan L, Tuck D, Harris L. The HDAC Inhibitor TSA Inhibits Cell Proliferation, Induces Apoptosis and Down-Regulates HER2 Protein and Gene Expression as a Single Agent and in Combination with Trastuzumab in Trastuzumab-Sensitive and -Resistant Breast Cancer Cell Lines. Cancer Research 2009, 69: 3133-3133. DOI: 10.1158/0008-5472.sabcs-09-3133.Peer-Reviewed Original ResearchRole of HDACiHistone deacetylase inhibitorsTrastuzumab-resistant breast cancerBreast cancerBreast cancer cell linesHER2 proteinCancer cell linesSingle agentResistant breast cancer cell linesCell linesHER2-positive breast cancerFirst biological therapyHER2 antibody trastuzumabValue of HER2Positive breast cancerTSA treatmentNormal breast epitheliumNormal breast cell lineAlternative therapeutic strategiesBreast cancer cellsGrowth inhibitory effectsInhibited cell survivalHDAC inhibitor trichostatinResistant cell linesMechanism of action
2005
Effect of combined treatment with methylprednisolone and soluble Nogo‐66 receptor after rat spinal cord injury
Ji B, Li M, Budel S, Pepinsky RB, Walus L, Engber TM, Strittmatter SM, Relton JK. Effect of combined treatment with methylprednisolone and soluble Nogo‐66 receptor after rat spinal cord injury. European Journal Of Neuroscience 2005, 22: 587-594. PMID: 16101740, PMCID: PMC2846292, DOI: 10.1111/j.1460-9568.2005.04241.x.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAxonsBehavior, AnimalBiotinCells, CulturedChick EmbryoDextransDisease Models, AnimalDose-Response Relationship, DrugDrug InteractionsDrug Therapy, CombinationExploratory BehaviorFemaleGanglia, SpinalGPI-Linked ProteinsImmunoglobulin GLaminectomyMethylprednisoloneMyelin ProteinsMyelin SheathNerve RegenerationNeuronsNogo Receptor 1Pyramidal TractsRatsRats, Long-EvansReceptors, Cell SurfaceReceptors, PeptideRecombinant ProteinsRecovery of FunctionSpinal Cord InjuriesConceptsSpinal cord injuryCord injuryRat spinal cord injuryMP treatmentAdult central nervous systemThoracic dorsal hemisectionNovel experimental therapiesCorticospinal tract axonsRecovery of functionNogo-66 receptorNumber of axonsCentral nervous systemGrowth inhibitory effectsDorsal hemisectionBBB scoresAxonal sproutingFunctional recoveryBresnahan (BBB) scoringAxonal regenerationMotor neuronsExperimental therapiesMethylprednisoloneSynthetic glucocorticoidNervous systemAxonal growth
2004
Restoration of Bone Morphogenetic Protein Receptor Type II Expression Leads to a Decreased Rate of Tumor Growth in Bladder Transitional Cell Carcinoma Cell Line TSU-Pr1
Kim I, Lee D, Lee D, Kim W, Kim M, Morton R, Lerner S, Kim S. Restoration of Bone Morphogenetic Protein Receptor Type II Expression Leads to a Decreased Rate of Tumor Growth in Bladder Transitional Cell Carcinoma Cell Line TSU-Pr1. Cancer Research 2004, 64: 7355-7360. PMID: 15492256, DOI: 10.1158/0008-5472.can-04-0154.Peer-Reviewed Original ResearchConceptsTSU-Pr1Cell line TSU-Pr1BMP-RIITumor growthBladder transitional cell carcinoma cellsHuman bladder cancer cell linesCell linesTransitional cell carcinoma cellsBladder cancer cell linesBone morphogenetic protein receptor type II (BMPR2) expressionBone morphogenetic proteinTSU-Pr1 cellsBladder TCC tissuesGrowth inhibitory effectsCancer cell linesBladder specimensType II expressionBladder TCCTumor gradeTransitional epitheliumClinical observationsTCC tissuesMalignant cellsSignificant associationBMP-RIA
2002
Arginine butyrate increases the cytotoxicity of DAB389IL-2 in leukemia and lymphoma cells by upregulation of IL-2Rβ gene
Shao RH, Tian X, Gorgun G, Urbano AG, Foss FM. Arginine butyrate increases the cytotoxicity of DAB389IL-2 in leukemia and lymphoma cells by upregulation of IL-2Rβ gene. Leukemia Research 2002, 26: 1077-1083. PMID: 12443879, DOI: 10.1016/s0145-2126(02)00059-0.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Combined Chemotherapy ProtocolsArginineButyratesCell SurvivalCyclic AMPDiphtheria ToxinDose-Response Relationship, DrugDrug SynergismHumansInterleukin-2Interleukin-2 Receptor beta SubunitLeukemiaLymphomaReceptors, InterleukinReceptors, Interleukin-2Recombinant Fusion ProteinsResponse ElementsSecond Messenger SystemsUp-RegulationConceptsCutaneous T-cell lymphomaIL-2R expressionNon-Hodgkin lymphomaArginine butyrateIL-2RLow affinity IL-2RHistone deacetylaseDirect growth-inhibitory effectB-cell non-Hodgkin lymphomaHigh-affinity IL-2 receptorLeukemia cellsCAMP response elementT-cell lymphomaIL-2 receptorNative diphtheria toxinGrowth inhibitory effectsClinical trialsP75 subunitAchievable concentrationsResponse rateVitro dataDAB389IL-2Interleukin-2 geneTumor cellsLymphoma cells
1996
Modulation of Sensitivity to Transforming Growth Factor-β1 (TGF-β1) and the Level of Type II TGF-β Receptor in LNCaP Cells by Dihydrotestosterone
Kim I, Zelner D, Sensibar J, Ahn H, Park L, Kim J, Lee C. Modulation of Sensitivity to Transforming Growth Factor-β1 (TGF-β1) and the Level of Type II TGF-β Receptor in LNCaP Cells by Dihydrotestosterone. Experimental Cell Research 1996, 222: 103-110. PMID: 8549651, DOI: 10.1006/excr.1996.0013.Peer-Reviewed Original ResearchMeSH KeywordsBinding, CompetitiveCell CountCell DivisionDihydrotestosteroneDNA, NeoplasmHumansMalePromoter Regions, GeneticProstatic NeoplasmsProtein Serine-Threonine KinasesReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaTranscriptional ActivationTransforming Growth Factor betaTumor Cells, CulturedConceptsTGF-beta receptor type IILNCaP cellsReceptor type IIAndrogen-responsive prostate cancerCharcoal-stripped fetal bovine serumEffect of dihydrotestosteroneGrowth factor-β1Type II TGF-β receptorProstate cancer cellsGrowth inhibitory effectsTGF-β receptorWestern blot analysisDHT concentrationsPresent studyType IIModulation of sensitivityProstate cancerAndrogenic conditionsFactor-β1DihydrotestosteronePotential physiological regulatorsInhibitory effectGene transcriptional activityCancer cellsPhysiological regulator
1989
RNA polymerase II transcripts as targets for 5-fluorouridine cytotoxicity: antagonism of 5-fluorouridine actions by α-amanitin
Heimer R, Sartorelli A. RNA polymerase II transcripts as targets for 5-fluorouridine cytotoxicity: antagonism of 5-fluorouridine actions by α-amanitin. Cancer Chemotherapy And Pharmacology 1989, 24: 80-86. PMID: 2731315, DOI: 10.1007/bf00263125.Peer-Reviewed Original ResearchMeSH KeywordsAdenosineAmanitinsCell DivisionCell Membrane PermeabilityChromatography, AffinityElectrophoresis, Agar GelHumansLeukemia, Erythroblastic, AcuteLysophosphatidylcholinesNucleic Acid HybridizationRNA Polymerase IIRNA PrecursorsRNA, MessengerTranscription, GeneticTumor Cells, CulturedTumor Stem Cell AssayUridineConceptsGrowth inhibitory effectsInhibitory effectΑ-amanitinColony formationFUrdCytotoxic consequencesSteady-state levelsAntagonismMRNAMRNA transcripts
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