0000000000065280

AUTHOR

Paula Ferrer

showing 6 related works from this author

Down-regulation of Glutathione and Bcl-2 Synthesis in Mouse B16 Melanoma Cells Avoids Their Survival during Interaction with the Vascular Endothelium

2003

B16 melanoma (B16M) cells with high GSH content show high metastatic activity. However, the molecular mechanisms linking GSH to metastatic cell survival are unclear. The possible relationship between GSH and the ability of Bcl-2 to prevent cell death was studied in B16M cells with high (F10) and low (F1) metastatic potential. Analysis of a Bcl-2 family of genes revealed that B16M-F10 cells, as compared with B16M-F1 cells, overexpressed preferentially Bcl-2 (approximately 5.7-fold). Hepatic sinusoidal endothelium-induced B16M-F10 cytotoxicity in vitro increased from approximately 19% (controls) to approximately 97% in GSH-depleted B16M-F10 cells treated with an antisense Bcl-2 oligodeoxynucl…

MaleProgrammed cell deathPore complexCell SurvivalMelanoma ExperimentalDown-RegulationOxidative phosphorylationBiologyBiochemistryOligodeoxyribonucleotides AntisenseMicechemistry.chemical_compoundDownregulation and upregulationCell Line TumorAnimalsButhionine SulfoximineMolecular BiologyBase SequenceTransition (genetics)Cell BiologyGlutathioneGlutathioneMolecular biologyGenes bcl-2Cell biologyMice Inbred C57BLOxidative StressCytosolchemistryEndothelium VascularEffluxCell DivisionJournal of Biological Chemistry
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Acceleration of glutathione efflux and inhibition of gamma-glutamyltranspeptidase sensitize metastatic B16 melanoma cells to endothelium-induced cyto…

2005

Highly metastatic B16 melanoma (B16M)-F10 cells, as compared with the low metastatic B16M-F1 line, have higher GSH content and preferentially overexpress BCL-2. In addition to its anti-apoptotic properties, BCL-2 inhibits efflux of GSH from B16M-F10 cells and thereby may facilitate metastatic cell resistance against endothelium-induced oxidative/nitrosative stress. Thus, we investigated in B16M-F10 cells which molecular mechanisms channel GSH release and whether their modulation may influence metastatic activity. GSH efflux was abolished in multidrug resistance protein 1 knock-out (MRP-/-1) B16M-F10 transfected with the Bcl-2 gene or in MRP-/-1 B16M-F10 cells incubated with l-methionine, wh…

MaleMelanoma ExperimentalCystic Fibrosis Transmembrane Conductance RegulatorApoptosisBiochemistryOligodeoxyribonucleotides Antisensechemistry.chemical_compoundMiceCell AdhesionAnimalsEndotheliumNeoplasm MetastasisCytotoxicityCell adhesionMolecular BiologybiologyActivator (genetics)Cell BiologyGlutathioneTransfectiongamma-GlutamyltransferaseMolecular biologyGlutathioneCystic fibrosis transmembrane conductance regulatorMice Inbred C57BLKineticsOxidative StresschemistryProto-Oncogene Proteins c-bcl-2VerapamilApoptosisbiology.proteinEffluxMultidrug Resistance-Associated ProteinsThe Journal of biological chemistry
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Bcl-2 and Mn-SOD antisense oligodeoxynucleotides and a glutamine-enriched diet facilitate elimination of highly resistant B16 melanoma cells by tumor…

2005

Mitochondrial glutathione (mtGSH) depletion increases sensitivity of Bcl-2-overexpressing B16 melanoma (B16M)-F10 cells (high metastatic potential) to tumor necrosis factor-alpha (TNF-alpha)-induced oxidative stress and death in vitro. In vivo, mtGSH depletion in B16M-F10 cells was achieved by feeding mice (where the B16M-F10 grew as a solid tumor in the footpad) with an L-glutamine (L-Gln)-enriched diet, which promoted in the tumor cells an increase in glutaminase activity, accumulation of cytosolic L-glutamate, and competitive inhibition of GSH transport into mitochondria. L-Gln-adapted B16M-F10 cells, isolated using anti-Met-72 monoclonal antibodies and flow cytometry-coupled cell sortin…

MaleProgrammed cell deathgovernment.form_of_governmentGlutamineSOD2Antineoplastic AgentsSoft Tissue NeoplasmsMitochondrionBiologyBiochemistryGlutaminase activitySuperoxide dismutaseMiceAnimalsMolecular BiologyMelanomaAntisense therapySuperoxide DismutaseTumor Necrosis Factor-alphaCell BiologyGenetic TherapyOligonucleotides AntisenseMolecular biologyAnimal FeedCombined Modality TherapyGlutathioneMitochondriaMice Inbred C57BLDisease Models AnimalOxidative StressMitochondrial permeability transition poreProto-Oncogene Proteins c-bcl-2Drug Resistance Neoplasmgovernmentbiology.proteinTumor necrosis factor alphaNeoplasm TransplantationThe Journal of biological chemistry
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Nitric Oxide Mediates Natural Polyphenol-induced Bcl-2 Down-regulation and Activation of Cell Death in Metastatic B16 Melanoma

2007

Intravenous administration to mice of trans-pterostilbene (t-PTER; 3,5-dimethoxy-4'-hydroxystilbene) and quercetin (QUER; 3,3',4',5,6-pentahydroxyflavone), two structurally related and naturally occurring small polyphenols, inhibits metastatic growth of highly malignant B16 melanoma F10 (B16M-F10) cells. t-PTER and QUER inhibit bcl-2 expression in metastatic cells, which sensitizes them to vascular endothelium-induced cytotoxicity. However, the molecular mechanism(s) linking polyphenol signaling and bcl-2 expression are unknown. NO is a potential bioregulator of apoptosis with controversial effects on Bcl-2 regulation. Polyphenols may affect NO generation. Short-term exposure (60 min/day) t…

MaleProgrammed cell deathCeramideEndotheliumDown-RegulationBiologyNitric OxideBiochemistryMicechemistry.chemical_compoundPhenolsCell Line TumorCell AdhesionmedicineAnimalsRNA MessengerNeoplasm MetastasisCytotoxicityMelanomaMolecular BiologyNitritesFlavonoidsNitratesCell DeathReverse Transcriptase Polymerase Chain ReactionPolyphenolsHydrogen PeroxideCell BiologyGenes bcl-2Cell biologyMice Inbred C57BLEndothelial stem cellmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Mitochondrial permeability transition porechemistryCell cultureApoptosisMitochondrial MembranesCancer researchEndothelium VascularJournal of Biological Chemistry
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Association between Pterostilbene and Quercetin Inhibits Metastatic Activity of B16 Melanoma

2005

AbstractInhibition of cancer growth by resveratrol (trans-3,5,4'trihydroxystilbene; RESV), a phytoalexin present in many plant species, is limited by its low bioavailability. Pterostilbene (3,5-dimethoxy-4'-hydroxystilbene; PTER) and quercetin (3,3',4',5,6-pentahydroxyflavone; QUER), two structurally related and naturally occurring small polyphenols, show longer half-life in vivo. In vitro growth of highly malignant B16 melanoma F10 cells (B16M-F10) is inhibited (56%) by short-time exposure (60 min/day) to PTER (40 μM) and QUER (20 μM) (approximate mean values of plasma concentrations measured within the first hour after intravenous administration of 20 mg/kg of each polyphenol). Intravenou…

Cancer ResearchpterostilbenePterostilbeneEndotheliumMelanomaPolyphenolsResveratrolPharmacologymedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282quercetinchemistry.chemical_compoundmedicine.anatomical_structurechemistryBiochemistryIn vivomedicinemelanomaVCAM-1Cell adhesionQuercetinmetastasesNeoplasia: An International Journal for Oncology Research
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Natural polyphenols facilitate elimination of HT-29 colorectal cancer xenografts by chemoradiotherapy: a Bcl-2- and superoxide dismutase 2-dependent …

2008

AbstractColorectal cancer is one of the most common malignancies worldwide. The treatment of advanced colorectal cancer with chemotherapy and radiation has two major problems: development of tumor resistance to therapy and nonspecific toxicity towards normal tissues. Different plant-derived polyphenols show anticancer properties and are pharmacologically safe. In vitro growth of human HT-29 colorectal cancer cells is inhibited (∼56%) by bioavailable concentrations of trans-pterostilbene (trans-3,5-dimethoxy-4′-hydroxystilbene; t-PTER) and quercetin (3,3′,4′,5,6-pentahydroxyflavone; QUER), two structurally related and naturally occurring small polyphenols. I.v. administration of t-PTER and Q…

Cancer ResearchAntioxidantColorectal cancerSp1 Transcription Factormedicine.medical_treatmentDown-RegulationMice NudeAntineoplastic AgentsBiologyAntioxidantsSuperoxide dismutaseMicePhenolsIn vivoGene expressionmedicineAnimalsHumansCell ProliferationFlavonoidsChemotherapySuperoxide DismutaseGene Expression ProfilingNF-kappa BPolyphenolsmedicine.diseaseChemotherapy regimenXenograft Model Antitumor AssaysOxaliplatinUp-RegulationOncologyBiochemistryProto-Oncogene Proteins c-bcl-2Drug Resistance NeoplasmCancer researchbiology.proteinFemaleColorectal NeoplasmsHT29 Cellsmedicine.drugMolecular cancer therapeutics
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