2020
Exosomes released by imatinib-resistant K562 cells contain specific membrane markers, IFITM3, CD146 and CD36 and increase the survival of imatinib-sensitive cells in the presence of imatinib
Hrdinova T, Toman O, Dresler J, Klimentova J, Salovska B, Pajer P, Bartos O, Polivkova V, Linhartova J, Machova Polakova K, Kabickova H, Brodska B, Krijt M, Zivny J, Vyoral D, Petrak J, Hrdinova T, Toman O, Dresler J, Klimentova J, Salovska B, Pajer P, Bartos O, Polivkova V, Linhartova J, Machova Polakova K, Kabickova H, Brodska B, Krijt M, Zivny J, Vyoral D, Petrak J. Exosomes released by imatinib-resistant K562 cells contain specific membrane markers, IFITM3, CD146 and CD36 and increase the survival of imatinib-sensitive cells in the presence of imatinib. International Journal Of Oncology 2020, 58: 238-250. PMID: 33491750, DOI: 10.3892/ijo.2020.5163.Peer-Reviewed Original ResearchConceptsTyrosine kinase inhibitorsChronic myeloid leukemiaImatinib-resistant K562 cellsCML therapyImatinib-sensitive K562 cellsDrug resistanceK562 cellsTargeted CML therapySubset of patientsLess common mutationsSpecific tyrosine kinase inhibitorTKI drug resistanceInterferon-induced transmembrane protein 3Presence of imatinibQuality of lifeMalignant hematopoietic disordersPotential diagnostic markerFlow cytometric analysisBCR-ABL1 geneConstitutive kinase activityCell surface markersLabel-free quantification proteomics analysisMutation-independent mechanismTransmembrane protein 3Development of resistance
2018
Radio-sensitizing effects of VE-821 and beyond: Distinct phosphoproteomic and metabolomic changes after ATR inhibition in irradiated MOLT-4 cells
Šalovská B, Janečková H, Fabrik I, Karlíková R, Čecháková L, Ondrej M, Link M, Friedecký D, Tichý A. Radio-sensitizing effects of VE-821 and beyond: Distinct phosphoproteomic and metabolomic changes after ATR inhibition in irradiated MOLT-4 cells. PLOS ONE 2018, 13: e0199349. PMID: 30001349, PMCID: PMC6042708, DOI: 10.1371/journal.pone.0199349.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid MotifsAtaxia Telangiectasia Mutated ProteinsBinding SitesBiomarkersCell Cycle CheckpointsCell Line, TumorComputational BiologyGamma RaysGene OntologyHumansMetabolomeMetabolomicsPhosphoproteinsPhosphorylationProtein BindingProtein Kinase InhibitorsProteomeProteomicsPyrazinesRadiation ToleranceRadiation-Sensitizing AgentsSignal TransductionSulfonesTOR Serine-Threonine KinasesConceptsVE-821MOLT-4 cellsCellular metabolismOncogene-induced replication stressATR inhibitionATM-deficient cellsDNA damage responseATR/Chk1 pathwayCell biology techniquesDownregulation of mTORAnti-cancer strategyCurrent anti-cancer strategiesReplication stressPhosphorylation sitesDamage responseIrradiation-induced oxidative stressQuantitative proteomicsDNA repairChk1 pathwayCellular eventsBiology techniquesSpecific inhibitorMain regulatorTumor-specific abnormalitiesMTOR inhibition
2015
Chemical inhibition of DNA repair kinases as a promising tool in oncology
Durisova K, Salovska B, Pejchal J, Tichy A. Chemical inhibition of DNA repair kinases as a promising tool in oncology. Biomedical Papers 2015, 160: 11-19. PMID: 26498210, DOI: 10.5507/bp.2015.046.Peer-Reviewed Original ResearchMeSH KeywordsAtaxia Telangiectasia Mutated ProteinsCDC2 Protein KinaseDNA Breaks, Double-StrandedDNA RepairDNA-Activated Protein KinaseHumansNeoplasmsProtein Kinase InhibitorsConceptsDNA-dependent protein kinaseDNA repair pathwaysRepair pathwaysDNA repairSpecific DNA repair pathwaysKey DNA repairDNA-damaging agentsSmall molecule inhibitorsATM-Rad3Protein kinaseAtaxia telangiectasiaChemical inhibitionKinaseMolecule inhibitorsSpecific inhibitorPathwayPotent inhibitorInhibitorsRecent studiesTumor resistanceTumor cellsMajor roleRadiotherapy efficiencyRepairCells
2014
Radiosensitization of Human Leukemic HL-60 Cells by ATR Kinase Inhibitor (VE-821): Phosphoproteomic Analysis
Šalovská B, Fabrik I, Ďurišová K, Link M, Vávrová J, Řezáčová M, Tichý A. Radiosensitization of Human Leukemic HL-60 Cells by ATR Kinase Inhibitor (VE-821): Phosphoproteomic Analysis. International Journal Of Molecular Sciences 2014, 15: 12007-12026. PMID: 25003641, PMCID: PMC4139827, DOI: 10.3390/ijms150712007.Peer-Reviewed Original ResearchMeSH KeywordsAtaxia Telangiectasia Mutated ProteinsCell Line, TumorGamma RaysHumansPhosphorylationProtein Kinase InhibitorsProteomePyrazinesRadiation-Sensitizing AgentsSulfonesConceptsDNA-dependent protein kinaseVE-821HL-60 cellsNano-liquid chromatography-tandem mass spectrometry analysisCell cycleSequence motif analysisDNA damage responseRadiation-induced double-strand breaksATR kinase inhibitorsDNA damage repairDNA damaging agentsHuman leukemic HL-60 cellsDouble-strand breaksSpecific ATR inhibitorActivity of kinasesInhibitor VE-821Leukemic HL-60 cellsCell cycle arrestQuantitative phosphoproteomicsATR kinaseMotif analysisPhosphorylation sitesCellular processesDamage responsePhosphoproteomic analysis
2013
Radio-sensitization of human leukaemic MOLT-4 cells by DNA-dependent protein kinase inhibitor, NU7441
Tichy A, Durisova K, Salovska B, Pejchal J, Zarybnicka L, Vavrova J, Dye N, Sinkorova Z. Radio-sensitization of human leukaemic MOLT-4 cells by DNA-dependent protein kinase inhibitor, NU7441. Radiation And Environmental Biophysics 2013, 53: 83-92. PMID: 24100951, DOI: 10.1007/s00411-013-0494-5.Peer-Reviewed Original ResearchConceptsDNA-dependent protein kinasePhosphorylation of H2A.XMOLT-4 cellsDNA-dependent protein kinase inhibitorDNA repair signalingProtein kinase inhibitorsAnti-apoptotic Mcl-1Cleavage of PARPHistone H2A.X.Cdc25A phosphataseProtein kinaseRepair signalingMolecular mechanismsNU7441Mcl-1Detection of IRDNA damageSpecific inhibitorPhosphorylationDetection of proteinsH2A.XSubsequent inductionKinase inhibitorsWestern blottingApoptosis