Search results for " Cell Line"

showing 10 items of 238 documents

Elimination of quiescent/slow-proliferating cancer stem cells by Bcl-XL inhibition in non-small cell lung cancer

2014

Lung cancer is the most common cause of cancer-related mortality worldwide, urging the discovery of novel molecular targets and therapeutic strategies. Stem cells have been recently isolated from non-small cell lung cancer (NSCLC), thus allowing the investigation of molecular pathways specifically active in the tumorigenic population. We have found that Bcl-XL is constantly expressed by lung cancer stem cells (LCSCs) and has a prominent role in regulating LCSC survival. Whereas chemotherapeutic agents were scarcely effective against LCSC, the small molecule Bcl-2/Bcl-XL inhibitor ABT-737, but not the selective Bcl-2 inhibitor ABT-199, induced LCSC death at nanomolar concentrations. Differen…

Lung NeoplasmsMice SCIDPharmacologyPiperazinesAntineoplastic AgentNitrophenolsMiceMice Inbred NODCarcinoma Non-Small-Cell LungCytotoxic T cellNon-Small-Cell Lungeducation.field_of_studySulfonamidesTumorAnimals; Antineoplastic Agents; Biphenyl Compounds; Carcinoma Non-Small-Cell Lung; Cell Line Tumor; Cell Proliferation; Cell Survival; Female; Humans; Lung Neoplasms; Mice Inbred NOD; Mice SCID; Neoplastic Stem Cells; Nitrophenols; Piperazines; Sulfonamides; Tumor Burden; Xenograft Model Antitumor Assays; bcl-X Protein; Molecular Biology; Cell BiologyTumor BurdenAnimals; Antineoplastic Agents; Biphenyl Compounds; Carcinoma Non-Small-Cell Lung; Cell Line Tumor; Cell Proliferation; Cell Survival; Female; Humans; Lung Neoplasms; Mice Inbred NOD; Mice SCID; Neoplastic Stem Cells; Nitrophenols; Piperazines; Sulfonamides; Tumor Burden; Xenograft Model Antitumor Assays; bcl-X ProteinNeoplastic Stem CellsFemaleStem cellHumanmedicine.drugXenograft Model Antitumor AssayCell SurvivalPopulationbcl-X ProteinAntineoplastic AgentsBiologySCIDSulfonamideCell LineCancer stem cellCell Line TumormedicineAnimalsHumanseducationLung cancerPiperazineMolecular BiologyCell ProliferationSettore MED/04 - Patologia GeneraleOriginal PaperNitrophenolAnimalCell growthCarcinomaBiphenyl CompoundsCell Biologymedicine.diseaseXenograft Model Antitumor AssaysGemcitabineLung NeoplasmCell cultureBiphenyl CompoundCancer researchInbred NODNeoplastic Stem Cell
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HSPH1 inhibition downregulates Bcl-6 and c-Myc and hampers the growth of human aggressive B-cell non-Hodgkin lymphoma

2015

We have shown that human B-cell non-Hodgkin lymphomas (B-NHLs) express heat shock protein (HSP)H1/105 in function of their aggressiveness. Here, we now clarify its role as a functional B-NHL target by testing the hypothesis that it promotes the stabilization of key lymphoma oncoproteins. HSPH1 silencing in 4 models of aggressive B-NHLs was paralleled by Bcl-6 and c-Myc downregulation. In vitro and in vivo analysis of HSPH1-silenced Namalwa cells showed that this effect was associated with a significant growth delay and the loss of tumorigenicity when 10(4) cells were injected into mice. Interestingly, we found that HSPH1 physically interacts with c-Myc and Bcl-6 in both Namalwa cells and pr…

Lymphoma B-CellXenograft Model Antitumor AssayDNA-Binding ProteinImmunologyDown-RegulationMice SCIDSettore MED/08 - Anatomia PatologicaBiologyBiochemistryHSP110 Heat-Shock ProteinProto-Oncogene Proteins c-mycMiceDownregulation and upregulationimmune system diseasesCell Line Tumorhemic and lymphatic diseasesHeat shock proteinGene Knockdown TechniquesmedicineAnimalsHumansGene silencingHSP110 Heat-Shock ProteinsAnimals; Cell Line Tumor; DNA-Binding Proteins; Down-Regulation; Gene Knockdown Techniques; HSP110 Heat-Shock Proteins; Humans; Lymphoma B-Cell; Mice; Mice SCID; Proto-Oncogene Proteins c-myc; Xenograft Model Antitumor Assays; Biochemistry; Immunology; Medicine (all); Hematology; Cell BiologyAnimalMedicine (all)Cell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysIn vitroLymphomaDNA-Binding ProteinsCell cultureGene Knockdown TechniquesGene Knockdown TechniqueImmunologyProto-Oncogene Proteins c-bcl-6Cancer researchB-Cell Non-Hodgkin LymphomaHumanBlood
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Differences in cell proliferation in rodent and human hepatic derived cell lines exposed to ciprofibrate.

2005

International audience; Humans appear to be refractory to some effects of peroxisome proliferators including alterations in cell proliferation, whereas rodents are susceptible. In this study, differences between the human and rat response to peroxisome proliferators were evaluated using rat and human tumour liver cell lines. Rat 7777 cells were more responsive than human HepG2 cells to ciprofibrate as they exhibited a higher decrease in cell number than HepG2, and underwent apoptosis. Results from these studies reveal a surprising response in tumour cell lines as the typical in vivo response of increased cell proliferation and reduced apoptosis was not observed in rat tumour cell lines at c…

MESH : Cell LineCancer ResearchRodentApoptosisMESH : Dose-Response Relationship DrugCell LineClofibric AcidIn vivobiology.animalmedicineMESH : Cell ProliferationAnimals[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCell ProliferationHypolipidemic AgentsDose-Response Relationship DrugbiologyCell growthMESH : RatsFibric AcidsMESH : LiverMESH : Clofibric AcidRatsCell biologyLiverOncologyApoptosisCell cultureHepg2 cellsCancer researchPeroxisome proliferator-activated receptor alphaCiprofibrateMESH : AnimalsMESH : Apoptosismedicine.drugMESH : Antilipemic Agents
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Trefoil factor TFF1-induced protection of conjunctival cells from apoptosis at premitochondrial and postmitochondrial levels.

2008

PURPOSE. Goblet cells of the conjunctival epithelium synthesize and secrete TFF1 (Trefoil factor 1), a small protease-resistant peptide that, together with mucins, is responsible for the rheologic properties of the tear film. This study aimed to determine whether TFF1, whose synthesis increases in inflammatory conditions such as pterygium, could protect conjunctival cells from apoptosis. METHODS. Chang conjunctival cells, either wild-type or expressing TFF1 through stable transfection, were exposed to benzalkonium chloride (BAK) and ultraviolet (UV) irradiation to trigger apoptosis. The authors used cell fractionation to detect lipid raft‐associated proteins, coimmunoprecipitation to explor…

MESH : Cell LineMESH : Chromosomes Human Pair 21Chromosomes Human Pair 21CellApoptosisMESH: Flow CytometryMESH: Caspase 8Membrane Potentials0302 clinical medicineMESH: Mitochondrial MembranesMESH: Chromosomes Human Pair 21MESH : Membrane Potentials0303 health sciencesCaspase 8MESH : Caspase 8MESH : Benzalkonium CompoundsMESH : Tumor Suppressor ProteinsChromosome MappingFas receptorFlow CytometryXIAPMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Epithelial Cells030220 oncology & carcinogenesisMitochondrial MembranesTrefoil Factor-1MESH : MitochondriaMESH : TransfectionBenzalkonium CompoundsConjunctivaMESH: Benzalkonium CompoundsProgrammed cell deathMESH: Enzyme ActivationMESH : ConjunctivaUltraviolet RaysMESH : Flow CytometryMESH: MitochondriaMESH: ConjunctivaCaspase 3BiologyInhibitor of apoptosisCaspase 8TransfectionCell Line03 medical and health sciencesMESH : Mitochondrial Membranesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansMESH: Membrane PotentialsMESH: Tumor Suppressor Proteins[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH: HumansTumor Suppressor ProteinsMESH: ApoptosisMESH: TransfectionMESH : HumansEpithelial CellsMolecular biologyMESH: Cell LineEnzyme ActivationApoptosisMESH : Ultraviolet RaysMESH: Ultraviolet RaysMESH : Enzyme ActivationMESH: Chromosome MappingMESH : ApoptosisMESH : Chromosome Mapping
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Effect of reducing agents on the acidification capacity and the proton motive force of Lactococcus lactis ssp. cremoris resting cells.

2002

International audience; Reducing agents are potential inhibitors of the microbial growth. We have shown recently that dithiothreitol (DTT), NaBH(4) and H(2) can modify the proton motive force of resting cells of Escherichia coli by increasing the membrane protons permeability [Eur. J. Biochem. 262 (1999) 595]. In the present work, the effect of reducing agents on the resting cells of Lactococcus lactis ssp. cremoris, a species widely employed in dairy processes was investigated. DTT did not affect the acidification nor the DeltapH, in contrast to the effect previously reported on E. coli. The DeltaPsi was slightly increased (30 mV) at low pH (pH 4) in the presence of 31 mM DTT or 2.6 mM NaB…

MESH : Cell LineMESH: Hydrogen-Ion ConcentrationMESH : DithioniteBorohydridesMESH : DithiothreitolBacterial growthmedicine.disease_causeMESH: Proton-Motive ForceDithiothreitolSodium dithionitechemistry.chemical_compoundMESH : Proton-Motive ForceElectrochemistry[INFO.INFO-BT]Computer Science [cs]/Biotechnology0303 health sciencesMESH : Interphasebiologyfood and beveragesProton-Motive ForceGeneral MedicineHydrogen-Ion ConcentrationMESH: BorohydridesLactococcus lactisMembraneBiochemistryReducing AgentsMESH : Sensitivity and SpecificityMESH : Reducing Agents[ INFO.INFO-BT ] Computer Science [cs]/BiotechnologyReducing agentMESH: Reducing AgentsBiophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologySensitivity and SpecificityCell LineMESH: Interphase03 medical and health sciencesSpecies SpecificityMESH : Hydrogen-Ion ConcentrationMESH: DithionitemedicineMESH : Species SpecificityMESH: Species SpecificityLactic AcidPhysical and Theoretical ChemistryEscherichia coli[SDV.BC] Life Sciences [q-bio]/Cellular BiologyInterphase030304 developmental biology[ SDV.BC ] Life Sciences [q-bio]/Cellular Biology030306 microbiologyChemiosmosisLactococcus lactisDithionitebiology.organism_classificationMESH: Sensitivity and SpecificityMESH: Cell LineDithiothreitol[INFO.INFO-BT] Computer Science [cs]/BiotechnologychemistryMESH: Lactococcus lactisMESH : BorohydridesMESH : Lactic AcidBiophysicsMESH: Lactic AcidMESH : Lactococcus lactisMESH: Dithiothreitol
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CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 immunology
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Sodium butyrate with UCN-01 has marked antitumour activity against cervical cancer cells.

2010

The effect of combining sodium butyrate (NaB), a histone deacetylase inhibitor, and 7-hydroxy-staurosporine (UCN-01) on cytotoxicity in human cervical carcinoma cells was evaluated.HeLa and CaSki cells were treated using NaB alone or in combination with staurosporine (STS) or its analog UCN-01. Cytotoxicity was determined by flow cytometry and morphological assays. Apoptotic pathways were characterized by Western blotting and immunostaining. CaSki cells were also xenografted into nude mice to assess the in vivo effects of NaB/UCN-01 combination.Treatment with NaB and STS or UCN-01 resulted in enhanced apoptosis of cancer cells. Apoptosis involved mitochondrial pathways and overexpression of…

MESH : StaurosporineMESH : Hela CellsMESH : Antineoplastic Combined Chemotherapy Protocolshealth care facilities manpower and servicesUterine Cervical NeoplasmsMESH: ButyratesMESH: Cell CycleApoptosisMESH: Papillomavirus Infections[ SDV.CAN ] Life Sciences [q-bio]/CancerMiceAntineoplastic Combined Chemotherapy ProtocolsMESH: AnimalsMESH: Human papillomavirus 18MESH : Human papillomavirus 18MESH : Femalehealth care economics and organizationsMESH: Human papillomavirus 16MESH : Papillomavirus InfectionsHuman papillomavirus 16Human papillomavirus 18Cell CycleMESH : Mice NudeMESH: Uterine Cervical NeoplasmsMESH: Antineoplastic Combined Chemotherapy ProtocolsButyratesMESH: Cell Growth ProcessesFemaleMESH: Xenograft Model Antitumor Assaysendocrine systemMESH: Cell Line TumoreducationMESH : Uterine Cervical NeoplasmsMice Nude[SDV.CAN]Life Sciences [q-bio]/CancerCell Growth ProcessesMESH : Xenograft Model Antitumor Assays[SDV.CAN] Life Sciences [q-bio]/CancerCell Line TumorMESH : ButyratesMESH : MiceMESH : Cell CycleMESH: Mice Nudeotorhinolaryngologic diseasesAnimalsHumansMESH: MiceMESH: HumansMESH : Cell Line TumorMESH: ApoptosisPapillomavirus InfectionsMESH : HumansMESH : Human papillomavirus 16StaurosporineXenograft Model Antitumor AssaysMESH: Hela CellsMESH : Cell Growth ProcessesMESH: StaurosporineMESH : AnimalsMESH: FemaleMESH : ApoptosisHeLa Cells
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Chemotherapy overcomes TRAIL-R4-mediated TRAIL resistance at the DISC level

2011

International audience; TNF-related apoptosis-inducing ligand or Apo2L (Apo2L/TRAIL) is a promising anti-cancer drug owing to its ability to trigger apoptosis by binding to TRAIL-R1 or TRAIL-R2, two membrane-bound receptors that are often expressed by tumor cells. TRAIL can also bind non-functional receptors such as TRAIL-R4, but controversies still exist regarding their potential to inhibit TRAIL-induced apoptosis. We show here that TRAIL-R4, expressed either endogenously or ectopically, inhibits TRAIL-induced apoptosis. Interestingly, the combination of chemotherapeutic drugs with TRAIL restores tumor cell sensitivity to apoptosis in TRAIL-R4-expressing cells. This sensitization, which ma…

MESH: CASP8 and FADD-Like Apoptosis Regulating ProteinMESH : Antineoplastic Combined Chemotherapy ProtocolsCASP8 and FADD-Like Apoptosis Regulating ProteinTRAILApoptosisMESH : Models BiologicalMitochondrionMESH : RNA Small InterferingMESH: Caspase 8TNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandMESH : Tumor Necrosis Factor Decoy Receptors0302 clinical medicineRNA interferenceNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsMESH: RNA Small InterferingMESH: NeoplasmsRNA Small InterferingReceptorSensitizationCaspase 80303 health sciencesMESH : Caspase 8MESH: Drug Resistance Neoplasm3. Good healthCell biologyMESH: Antineoplastic Combined Chemotherapy ProtocolsMESH : Drug Resistance Neoplasmmedicine.anatomical_structure030220 oncology & carcinogenesisRNA InterferenceMESH : GPI-Linked ProteinsMESH: TNF-Related Apoptosis-Inducing LigandDeath Domain Receptor Signaling Adaptor ProteinsProgrammed cell deathMESH: Cell Line Tumorc-FLIPMESH: RNA InterferenceBiologyGPI-Linked ProteinsCaspase 8Models Biological03 medical and health sciencesCell Line TumorReceptors Tumor Necrosis Factor Member 10cmedicineTRAIL-R4HumanscancerChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology030304 developmental biologyOriginal PaperMESH: HumansMESH : Cell Line TumorMESH: ApoptosisMESH : HumansMESH: Models BiologicalMESH : CASP8 and FADD-Like Apoptosis Regulating ProteinCell BiologyMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : NeoplasmsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsDrug Resistance NeoplasmApoptosisMESH : RNA InterferenceMESH: GPI-Linked ProteinsMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsMESH: Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy Receptors
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Vezatin, a novel transmembrane protein, bridges myosin VIIA to the cadherin-catenins complex

2000

International audience; Defects in myosin VIIA are responsible for deafness in the human and mouse. The role of this unconventional myosin in the sensory hair cells of the inner ear is not yet understood. Here we show that the C-terminal FERM domain of myosin VIIA binds to a novel transmembrane protein, vezatin, which we identi®ed by a yeast two-hybrid screen. Vezatin is a ubiquitous protein of adherens cell±cell junctions, where it interacts with both myosin VIIA and the cadherin±catenins complex. Its recruitment to adherens junctions implicates the C-terminal region of a-catenin. Taken together, these data suggest that myosin VIIA, anchored by vezatin to the cadherin±catenins complex, cre…

MESH: Cytoskeletal ProteinsMESH: alpha CateninStereocilia (inner ear)[SDV]Life Sciences [q-bio]MESH: Amino Acid SequenceDeafnessMESH: CadherinsMiceMESH: Protein Structure Tertiary0302 clinical medicine[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesMyosinMESH: Hair Cells AuditoryMESH: AnimalsCytoskeleton0303 health sciencesFERM domainGeneral NeuroscienceMESH: Alternative SplicingArticlesCadherinsCell biologymedicine.anatomical_structureIntercellular Junctions[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyMyosin VIIaHair cellMESH: Membrane ProteinsMESH: DyneinsProtein BindingMESH: MutationMacromolecular SubstancesMolecular Sequence DataMESH: Deafnessmacromolecular substancesBiologyIn Vitro TechniquesMyosinsGeneral Biochemistry Genetics and Molecular BiologyCell LineAdherens junction03 medical and health sciencesHair Cells Auditorymedicineotorhinolaryngologic diseasesAnimalsHumansMESH: Myosin VIIaMESH: Protein BindingAmino Acid SequenceMolecular BiologyMESH: Mice030304 developmental biologyMESH: In Vitro TechniquesMESH: Molecular Sequence DataMESH: HumansGeneral Immunology and MicrobiologyCadherinDyneinsMembrane ProteinsMESH: Macromolecular SubstancesMESH: MyosinsActin cytoskeleton[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyProtein Structure TertiaryMESH: Cell LineAlternative SplicingCytoskeletal ProteinsMutationsense organs030217 neurology & neurosurgeryalpha Catenin[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyMESH: Intercellular Junctions
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S-nitrosylation of the death receptor fas promotes fas ligand-mediated apoptosis in cancer cells.

2011

International audience; BACKGROUND & AIMS: Fas belongs to the family of tumor necrosis factor receptors which induce apoptosis. Many cancer cells express Fas but do not undergo Fas-mediated apoptosis. Nitric oxide reverses this resistance by increasing levels of Fas at the plasma membrane. We studied the mechanisms by which NO affects Fas function. METHODS: Colon and mammary cancer cell lines were incubated with the NO donor glyceryl trinitrate or lipid A; S-nitrosylation of Fas was monitored using the biotin switch assay. Fas constructs that contained mutations at cysteine residues that prevent S-nitrosylation were used to investigate the involvement of S-nitrosylation in Fas-mediated cell…

MESH: NitroglycerinMESH: Signal TransductionTime FactorsMESH: Membrane MicrodomainsApoptosisMESH : Fas Ligand ProteinCytoplasmic partMESH: Lipid AFas ligandMiceNitroglycerin0302 clinical medicineMESH : Protein TransportMESH : FemaleMESH: AnimalsFADDLipid raft0303 health sciencesTumorbiologyColon CancerMESH : Lipid AMESH : BiotinylationGastroenterologyFas receptorMESH: Antigens CD95Protein TransportLipid AMESH : Colonic NeoplasmsMESH : Nitric OxideMESH : Nitric Oxide Donors030220 oncology & carcinogenesisColonic NeoplasmsDeath-inducing signaling complexFemale[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH : MutationMESH : TransfectionSignal TransductionMESH : Time FactorsMESH: Protein TransportFas Ligand ProteinMESH : Mammary Neoplasms ExperimentalMESH: MutationMESH: Cell Line TumorMESH: Mammary Neoplasms ExperimentalNitric OxideTransfectionCaspase 803 medical and health sciencesMembrane MicrodomainsCell Line TumorMESH : MiceAnimalsHumansBiotinylationNitric Oxide DonorsMESH: BiotinylationCysteinefas ReceptorMESH: MiceMESH : Protein Processing Post-Translational030304 developmental biologyMESH : Signal TransductionMESH: Colonic NeoplasmsMESH : CysteineMESH: HumansHepatologyMESH : Cell Line TumorMESH: ApoptosisMESH: TransfectionMESH : HumansMESH: Time FactorsMammary Neoplasms Experimental[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: CysteineMESH: Nitric Oxide DonorsMolecular biologySignalingMESH: Fas Ligand ProteinMESH : NitroglycerinApoptosisLocalizationMESH: Nitric OxideMESH: Protein Processing Post-TranslationalMutationbiology.proteinMESH : Membrane MicrodomainsMESH : AnimalsMESH : Antigens CD95Protein Processing Post-TranslationalMESH: FemaleMESH : Apoptosis
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