2003
Kahalalide F, a new marine-derived compound, induces oncosis in human prostate and breast cancer cells.
Suárez Y, González L, Cuadrado A, Berciano M, Lafarga M, Muñoz A. Kahalalide F, a new marine-derived compound, induces oncosis in human prostate and breast cancer cells. Molecular Cancer Therapeutics 2003, 2: 863-72. PMID: 14555705.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid Chloromethyl KetonesApoptosisBreast NeoplasmsCaspase InhibitorsCaspasesCell CycleCell NucleusCell Transformation, NeoplasticCysteine Proteinase InhibitorsDepsipeptidesFemaleFlow CytometryHumansLysosomesMaleMollusk VenomsOligopeptidesPeptidesProstatic NeoplasmsTumor Cells, CulturedConceptsAnti-apoptotic Bcl-2 proteinGeneral caspase inhibitorSevere cytoplasmic swellingMitochondrial membrane potentialCell cycle arrestBcl-2 proteinKahalalide FTranslation inhibitorsMarine-derived compoundsNuclear domainsCaspase inhibitorsNuclear envelopeNew marine-derived compoundDNA degradationEndoplasmic reticulumHuman cellsCell deathNovel antitumor drugsBreast cancer cellsJC-1LysoTracker GreenCell nucleiBreast cancer cell linesCancer cell linesMitochondrial damage
2002
AplidinTM Induces Apoptosis in Human Cancer Cells via Glutathione Depletion and Sustained Activation of the Epidermal Growth Factor Receptor, Src, JNK, and p38 MAPK*
Cuadrado A, Garcı́a-Fernández L, González L, Suárez Y, Losada A, Alcaide V, Martı́nez T, Fernández-Sousa J, Sánchez-Puelles J, Muñoz A. AplidinTM Induces Apoptosis in Human Cancer Cells via Glutathione Depletion and Sustained Activation of the Epidermal Growth Factor Receptor, Src, JNK, and p38 MAPK*. Journal Of Biological Chemistry 2002, 278: 241-250. PMID: 12414812, DOI: 10.1074/jbc.m201010200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsApoptosisBreast NeoplasmsCell DivisionCell SurvivalCells, CulturedDepsipeptidesEnzyme ActivationEnzyme InhibitorsErbB ReceptorsFemaleFibroblastsFlow CytometryGlutathioneHumansJNK Mitogen-Activated Protein KinasesKidney NeoplasmsMiceMitogen-Activated Protein KinasesP38 Mitogen-Activated Protein KinasesPeptides, CyclicPhosphorylationProto-Oncogene Proteins pp60(c-src)Receptors, Platelet-Derived Growth FactorTumor Cells, CulturedConceptsEpidermal growth factor receptorP38 MAPK activationP38 MAPKNon-receptor protein tyrosine kinase SrcGrowth factor receptorMAPK activationProtein tyrosine kinase SrcStress response programSustained activationFactor receptorCancer cellsMDA-MB-231 breast cancer cellsHuman cancer cellsBenzyloxycarbonyl-VADKinase SrcHuman MDA-MB-231 breast cancer cellsMDA-MB-231 cellsMolecular basisKinase JNKPretreatment of cellsMouse embryosEGFR activationFluoromethyl ketoneGrowth arrestHuman renal cancer
1999
Impact of different low-density lipoprotein (LDL) receptor mutations on the ability of LDL to support lymphocyte proliferation
Martínez-Botas J, Suárez Y, Reshef A, Carrero P, Ortega H, Gómez-Coronado D, Teruel J, Leitersdorf E, Lasunción M. Impact of different low-density lipoprotein (LDL) receptor mutations on the ability of LDL to support lymphocyte proliferation. Metabolism 1999, 48: 834-839. PMID: 10421221, DOI: 10.1016/s0026-0495(99)90214-7.Peer-Reviewed Original ResearchConceptsLow-density lipoproteinAbility of LDLFamilial hypercholesterolemiaReceptor mutationsLow-density lipoprotein receptor mutationNormal low density lipoproteinHomozygous familial hypercholesterolemiaDifferent LDL receptor mutationsEndogenous cholesterol synthesisLDL receptor mutationsMitogen-stimulated lymphocytesLymphocyte proliferationPeripheral lymphocytesLDL particlesLymphocytesMitogenic effectCytometric analysisCholesterol synthesisLDL bindingCase 2Case 1Similar extentCompound heterozygotesDefective internalizationDifferent phenotypes
1998
Induction of apoptosis in p53-null HL-60 cells by inhibition of lanosterol 14-α demethylase
Martínez-Botas J, Ferruelo A, Suárez Y, Gómez-Coronado D, Lasunción M. Induction of apoptosis in p53-null HL-60 cells by inhibition of lanosterol 14-α demethylase. Biochimie 1998, 80: 887-894. PMID: 9893947, DOI: 10.1016/s0300-9084(00)88884-7.Peer-Reviewed Original Research