2006
Vitamin D regulates the phenotype of human breast cancer cells
Pendás-Franco N, González-Sancho J, Suárez Y, Aguilera O, Steinmeyer A, Gamallo C, Berciano MT, Lafarga M, Muñoz A. Vitamin D regulates the phenotype of human breast cancer cells. Differentiation 2006, 75: 193-207. PMID: 17288543, DOI: 10.1111/j.1432-0436.2006.00131.x.Peer-Reviewed Original ResearchConceptsSmooth muscle alpha-actinFocal adhesion kinaseBreast cancer cellsHuman breast cancer cellsCancer cellsP-cadherinFocal adhesion plaquesMDA-MB-453Muscle alpha-actinMesenchymal markers N-cadherinMDA-MB-468 cellsAdhesion kinasePlasma membraneAdhesion plaquesMDA-MB-453 cellsLarge cytoplasmic extensionsActin filamentsE-cadherin expressionCell adhesionCell typesN-cadherinAlpha-actinBreast cancer cell linesCancer cell linesLaser confocalPlitidepsin Cellular Binding and Rac1/JNK Pathway Activation Depend on Membrane Cholesterol Content
Suárez Y, González-Santiago L, Zarich N, Dávalos A, Aranda JF, Alonso MA, Lasunción MA, Rojas JM, Muñoz A. Plitidepsin Cellular Binding and Rac1/JNK Pathway Activation Depend on Membrane Cholesterol Content. Molecular Pharmacology 2006, 70: 1654-1663. PMID: 16928956, DOI: 10.1124/mol.106.025569.Peer-Reviewed Original ResearchConceptsJun N-terminal kinaseMembrane cholesterol contentRac1-JNK pathwayHeLa cellsWild-type HeLa cellsMembrane-bound Rac1Plasma membrane cholesterolRac1 small GTPaseN-terminal kinaseMKP-1 phosphataseJNK pathway activationCellular bindingMDA-MB-231 breast cancer cellsInduction of apoptosisSmall GTPaseMarine cyclic depsipeptidePlasma membraneJNK activationRac1 activationMembrane cholesterolCell deathSubcellular fractioningBreast cancer cellsSustained activationRac1
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 cancerInhibition of cholesterol biosynthesis by Δ22-unsaturated phytosterols via competitive inhibition of sterol Δ24-reductase in mammalian cells
FERNÁNDEZ C, SUÁREZ Y, FERRUELO AJ, GÓMEZ-CORONADO D, LASUNCIÓN MA. Inhibition of cholesterol biosynthesis by Δ22-unsaturated phytosterols via competitive inhibition of sterol Δ24-reductase in mammalian cells. Biochemical Journal 2002, 366: 109-119. PMID: 12162789, PMCID: PMC1222779, DOI: 10.1042/bj20011777.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding, CompetitiveCaco-2 CellsCholesterolChromatography, High Pressure LiquidDose-Response Relationship, DrugHL-60 CellsHumansHypolipidemic AgentsKineticsMacrophagesMaleMiceMicrosomes, LiverModels, ChemicalOxidoreductasesPhytosterolsRatsRats, Sprague-DawleyStigmasterolTime FactorsTumor Cells, CulturedConceptsCholesterol biosynthesisCholesterol-lowering actionCholesterol-lowering agentsEffective hypocholesterolaemic agentHL-60 human cell linesRat liver microsomesIntestinal absorptionDietary phytosterolsLiver microsomesHypocholesterolaemic agentsLow intracellular concentrationsCaco-2Inhibition of sterolIncorporation of radioactivityHuman cell linesCell linesInhibitionSaturated side chainIntracellular concentrationCholesterolRelevant concentrationsRadioactivity incorporationPresent studyStrong inhibitionCompetitive inhibition