Search results for "MESH: Apoptosis"

showing 6 items of 16 documents

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
researchProduct

TRAIL in cancer therapy: present and future challenges.

2007

International audience; Since its identification in 1995, TNF-related apoptosis-inducing ligand (TRAIL) has sparked growing interest in oncology due to its reported ability to selectively trigger cancer cell death. In contrast to other members of the TNF superfamily, TRAIL administration in vivo is safe. The relative absence of toxic side effects of this naturally occurring cytokine, in addition to its antitumoural properties, has led to its preclinical evaluation. However, despite intensive investigations, little is known in regards to the mechanisms underlying TRAIL selectivity or efficiency. An appropriate understanding of its physiological relevance, and of the mechanisms controlling ca…

MESH: Signal Transductionmedicine.medical_treatmentClinical BiochemistryApoptosisTRAILTNF-Related Apoptosis-Inducing LigandBioinformaticsTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing Ligand0302 clinical medicineDrug Delivery SystemsNeoplasmsDrug DiscoveryMESH: AnimalsMESH: Neoplasms0303 health sciencesTnf superfamily3. Good healthMESH : Antineoplastic AgentsCytokine030220 oncology & carcinogenesisMolecular MedicineMESH : Drug Delivery SystemsTRAIL-Receptors.Signal transductionMESH: TNF-Related Apoptosis-Inducing LigandSignal TransductionMESH: ForecastingProgrammed cell deathMESH: Drug Delivery SystemsCancer therapyAntineoplastic AgentsArticleresistance03 medical and health sciencesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsHumanscancer[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : ForecastingTRAIL-receptor agonistic antibodies[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyPharmacologyMESH : Signal TransductionMESH: Humansbusiness.industryMESH: ApoptosisMESH : HumansCancermedicine.diseaseMESH : NeoplasmsCancer cellImmunologyMESH: Antineoplastic AgentsMESH : AnimalsbusinessTRAIL-ReceptorsMESH : ApoptosisForecasting
researchProduct

The columnar gene vnd is required for tritocerebral neuromere formation during embryonic brain development of Drosophila.

2006

International audience; In Drosophila, evolutionarily conserved transcription factors are required for the specification of neural lineages along the anteroposterior and dorsoventral axes, such as Hox genes for anteroposterior and columnar genes for dorsoventral patterning. In this report, we analyse the role of the columnar patterning gene ventral nervous system defective (vnd) in embryonic brain development. Expression of vnd is observed in specific subsets of cells in all brain neuromeres. Loss-of-function analysis focussed on the tritocerebrum shows that inactivation of vnd results in regionalized axonal patterning defects, which are comparable with the brain phenotype caused by mutatio…

Nervous systemMutantApoptosis0302 clinical medicineMESH: Gene Expression Regulation DevelopmentalDrosophila ProteinsMESH: AnimalsAxonHox geneMESH: MelatoninGenetics0303 health sciencesMESH: Pineal GlandBrainGene Expression Regulation DevelopmentalMESH: Transcription FactorsNeuromerePhenotypeBiological EvolutionCell biologymedicine.anatomical_structureDrosophila melanogasterPhenotypeMESH: Photic StimulationMESH: Body PatterningMESH: MutationMESH: Drosophila ProteinsBiologyMESH: PhenotypeMESH: Drosophila melanogaster03 medical and health sciencesMESH: BrainNeuroblastMESH: EvolutionMESH: Homeodomain ProteinsmedicineAnimalsMESH: Circadian RhythmMolecular Biology030304 developmental biologyBody PatterningHomeodomain ProteinsMESH: HumansMESH: ApoptosisEmbryogenesis[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMESH: LightMutationMESH: SerotoninMESH: Seasons030217 neurology & neurosurgeryDevelopmental BiologyTranscription Factors
researchProduct

Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
researchProduct

A role for peroxisome proliferator-activated receptor gamma in resveratrol-induced colon cancer cell apoptosis.

2014

Scope Resveratrol may function as a chemopreventive agent. A recent clinical study demonstrates a reduction in tumor cell proliferation in colorectal patients receiving repeated oral ingestion of resveratrol. However, gaps remain in our knowledge of the molecular mechanisms by which resveratrol exerts its chemopreventive effect. We have previously demonstrated that resveratrol induces apoptosis in colon cancer cells and that resveratrol can sensitize chemoresistant colon cancer cells to various drugs. Based on its ability to activate peroxisome proliferator-activated receptor gamma (PPARγ) in colon cancer cells, we sought to determine the implication of this nuclear transcription factor in …

endocrine system diseasesColorectal cancerPeroxisome proliferator-activated receptorApoptosisPharmacologyResveratrolresveratrolMESH: ThiazolidinedionesPPAR[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compound0302 clinical medicineMESH: StilbenesStilbenesMESH : Cell Proliferation[ SHS.INFO ] Humanities and Social Sciences/Library and information sciencesAnilidesskin and connective tissue diseaseschemistry.chemical_classification0303 health sciencesfood and beveragesCell cycle3. Good healthMESH : ThiazolidinedionesMESH : Colonic Neoplasmscolon cancer030220 oncology & carcinogenesisColonic NeoplasmsS Phase Cell Cycle CheckpointsRosiglitazonehormones hormone substitutes and hormone antagonistsBiotechnologymedicine.drugMESH : PPAR gammaMESH: Cell Line Tumor[SHS.INFO]Humanities and Social Sciences/Library and information sciences[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: Anilides[SHS.INFO] Humanities and Social Sciences/Library and information sciencesMESH : AnilidesMESH : StilbenesRosiglitazone03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerCell Line TumorMESH: Cell Proliferationmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular BiologyMESH : S Phase Cell Cycle Checkpoints[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologypolyphenols030304 developmental biologyCell ProliferationMESH: Colonic NeoplasmsMESH: HumansCell growthMESH : Cell Line Tumor[ SDV.BC ] Life Sciences [q-bio]/Cellular Biologyorganic chemicalsMESH: ApoptosisMESH : Humansmedicine.diseasePPAR gammaMESH: S Phase Cell Cycle CheckpointschemistryMESH: PPAR gammaApoptosisCancer cellThiazolidinedionesMESH : ApoptosisFood Science
researchProduct

Mechanisms involved in lipid accumulation and apoptosis induced by 1-nitropyrene in Hepa1c1c7 cells

2011

International audience; 1-Nitropyrene (1-NP) is a nitro-polycyclic aromatic hydrocarbon (nitro-PAH) present in diesel exhaust and bound to particular matter in urban air. We show that 1-NP and the referent PAH benzo(a)pyrene (BP) induce apoptosis and a lipid accumulation dependent on cytochrome P450 1A1-metabolites in mouse hepatoma cells, whereas 1-amino-pyrene had no effect. The caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethyl ketone (Z-VAD-fmk), inhibits 1-NP-induced apoptosis, but failed to alter 1-NP-triggered lipid accumulation determined by Nile red staining. We further show that cholesterol and fatty acid contents are modified after nitro-PAH exposure and that 1…

endoplasmic-reticulum stressMESH: PyrenesHepatoma cellsliver-cellsactivated protein-kinaseApoptosisAMP-Activated Protein KinasesToxicologyMESH: Liver Neoplasms ExperimentalMicechemistry.chemical_compoundMESH: CholesterolLiver Neoplasms ExperimentalMESH: AnimalsMESH: AMP-Activated Protein KinasesStearoyl-CoA desaturase 1CaspaseMESH: Lipid Metabolismchemistry.chemical_classificationhuman macrophages0303 health sciencesPyrenesbiology8-tetrachlorodibenzo-p-dioxin tcdd030302 biochemistry & molecular biologyGeneral Medicineinhibition[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]CholesterolBiochemistry[SDV.TOX]Life Sciences [q-bio]/ToxicologyCaspaseslipids (amino acids peptides and proteins)stearoyl-coaStearoyl-CoA DesaturaseMESH: Cell Line Tumor[SDV.BC]Life Sciences [q-bio]/Cellular Biology03 medical and health sciencesMESH: Benzo(a)pyreneCell Line Tumor1-NitropyreneBenzo(a)pyreneAnimalsFatty acidsProtein kinase AMESH: Mice030304 developmental biologyaromatic-hydrocarbonsMESH: CaspasesCholesterolMESH: Apoptosisc-srcFatty acidAMPKCytochrome P450Lipid MetabolismMolecular biologychemistryApoptosisMESH: Stearoyl-CoA Desaturasebiology.proteinStearoyl-CoA desaturase-1desaturaseToxicology Letters
researchProduct