Search results for " apoptosis."

showing 10 items of 359 documents

3-Deazaneplanocin A (DZNep), an Inhibitor of the Histone Methyltransferase EZH2, Induces Apoptosis and Reduces Cell Migration in Chondrosarcoma Cells

2014

Objective Growing evidences indicate that the histone methyltransferase EZH2 (enhancer of zeste homolog 2) may be an appropriate therapeutic target in some tumors. Indeed, a high expression of EZH2 is correlated with poor prognosis and metastasis in many cancers. In addition, 3-Deazaneplanocin A (DZNep), an S-adenosyl-L homocysteine hydrolase inhibitor which induces EZH2 protein depletion, leads to cell death in several cancers and tumors. The aim of this study was to determine whether an epigenetic therapy targeting EZH2 with DZNep may be also efficient to treat chondrosarcomas. Methods EZH2 expression was determined by immunohistochemistry and western-blot. Chondrosarcoma cell line CH2879…

MESH: Cell DeathAdenosine[SDV]Life Sciences [q-bio]Cancer Treatmentlcsh:MedicineMESH: Flow CytometryApoptosischemistry.chemical_compoundSpectrum Analysis Techniques0302 clinical medicineCell MovementMolecular Cell BiologyMedicine and Health Sciences3-Deazaneplanocin AMESH: Epigenesis GeneticEnzyme Inhibitorslcsh:Science0303 health sciencesMultidisciplinaryCell DeathbiologyReverse Transcriptase Polymerase Chain ReactionEZH2Polycomb Repressive Complex 2DrugsCell migrationMESH: ChondrosarcomaFlow Cytometry3. Good healthHistone[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemOncologyConnective TissueCell ProcessesSpectrophotometry030220 oncology & carcinogenesisHistone methyltransferaseHistone MethyltransferasesMESH: 3-deazaneplanocinCytophotometryAnatomyMESH: Polycomb Repressive Complex 2Epigenetic therapyMESH: Histone methyltransferaseResearch ArticleProgrammed cell deathHistologyChondrosarcoma[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular Biologymacromolecular substancesResearch and Analysis MethodsCell GrowthEpigenetic Therapy03 medical and health sciencesRheumatologyCell Line TumorMESH: Blotting WesternHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEZH2Tumors030304 developmental biologyMESH: Apoptosislcsh:RMESH: Histone-Lysine N-MethyltransferaseBiology and Life SciencesMESH: ImmunohistochemistryHistone-Lysine N-MethyltransferaseCell BiologyBiological TissueCartilageHistone methyltransferasechemistryApoptosisbiology.proteinCancer researchMESH: EZH2 protein humanlcsh:QCytometry
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Early mitochondrial dysfunction, superoxide anion production, and DNA degradation are associated with non-apoptotic death of human airway epithelial …

2002

It has been shown that bacterial exoproducts may induce airway epithelium injury. During the epithelial repair process, the respiratory epithelial cells no more establish tight junctional intercellular complexes and may be particularly susceptible to bacterial virulence factors. In this study, we analyzed the effect of Pseudomonas aeruginosa exotoxin A (ETA) at different periods of time and concentrations on 16 HBE 14o(-) human bronchial epithelial cells in culture conditions inducing a phenotype of repairing cells. ETA treatment for 24 and 48 h led to the killing of 40.0 +/- 5.7% and 79.0 +/- 1.4% of the cells, respectively, as determined by the dimethylthiazole 2,5 diphenyl tetrazolium br…

MESH: Cell DeathMESH: ADP Ribose TransferasesMESH : DNAClinical BiochemistryCellApoptosisMESH : Dose-Response Relationship DrugMitochondrion[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractMembrane PotentialsMESH: Dose-Response Relationship Drugchemistry.chemical_compoundSuperoxidesMESH: Intracellular MembraneMESH : DNA FragmentationRespiratory systemEnzyme InhibitorsCells CulturedADP Ribose TransferasesMESH : Cell SurvivalCell DeathSuperoxideMESH: DNAMESH: BronchiCaspase InhibitorsMESH : BronchiMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Cell SurvivalMESH: Enzyme InhibitorsMESH: Epithelial CellsMESH : ADP Ribose TransferasesIntracellularMESH: Cells CulturedPulmonary and Respiratory MedicineProgrammed cell deathCell SurvivalVirulence FactorsBacterial ToxinsExotoxinsBronchiDNA FragmentationRespiratory MucosaBiologyMicrobiologyNecrosisNasal PolypsMESH : Cells CulturedmedicineHumansMESH: DNA FragmentationMESH : Intracellular MembraneMolecular BiologyMESH : Enzyme InhibitorsMESH: HumansMESH: CaspasesDose-Response Relationship DrugMESH: ApoptosisMESH : HumansEpithelial CellsCell BiologyDNAIntracellular MembranesMESH: ExotoxinschemistryMESH: Bacterial ToxinsApoptosisMESH : ExotoxinsMESH : Cell DeathMESH : Bacterial ToxinsRespiratory epithelium[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractMESH : CaspasesMESH : Apoptosis[ SDV.MHEP.PSR ] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract
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Regulating TRAIL Receptor-Induced Cell Death at the Membrane: A Deadly Discussion

2011

Article Open access plus; International audience; The use of TRAIL/APO2L and monoclonal antibodies targeting TRAIL receptors for cancer therapy holds great promise, due to their ability to restore cancer cell sensitivity to apoptosis in association with conventional chemotherapeutic drugs in a large variety of tumors. TRAIL-induced cell death is tightly regulated right from the membrane and at the DISC (Death-Inducing Signaling Complex) level. The following patent and literature review aims to present and highlight recent findings of the deadly discussion that determines tumor cell fate upon TRAIL engagement.

MESH: Cell DeathMESH: Signal TransductionCancer ResearchApoptosisTRAILMESH : Models BiologicalscaffoldCell membrane0302 clinical medicineDrug DiscoveryMESH: AnimalsPharmacology (medical)Receptordeath effector domain0303 health sciencesCell DeathGeneral MedicineTRAIL-R4.3. Good healthCell biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisSignal transductionMESH : Apoptosis Regulatory ProteinsSignal TransductionProgrammed cell deathc-FLIPdeath domainmedicine.drug_classMESH : Cell MembraneCancer therapyBiologyMonoclonal antibodyModels BiologicalArticle03 medical and health sciencesmedicineAnimalsHumansChemotherapy[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 Biology030304 developmental biologyMESH : Signal TransductionMESH: HumansMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell MembraneMESH: Models BiologicalDISCReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMESH : Cell DeathFADDCancer cellMESH : AnimalsApoptosis Regulatory ProteinsMESH : ApoptosisMESH: Cell MembraneRecent Patents on Anti-Cancer Drug Discovery
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Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

2009

Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases. Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies. It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios. Thus far, dozens of methods have been proposed to quantify cell death-related parameters. However, no guid…

MESH: Cell DeathcytofluorometryMESH : Microscopy Fluorescenceved/biology.organism_classification_rank.speciesCellMESH: Flow CytometryMESH: Microscopy FluorescenceApoptosisfluorescence microscopyMESH: Eukaryotic CellsAnnexin Vnecrosis0302 clinical medicineEukaryotic Cells/cytologyMitochondrial membrane permeabilizationScanningMESH : ImmunoblottingGeneticsApoptosis; Cell Death; Eukaryotic Cells/cytology; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence0303 health sciencesMicroscopyMESH : Spectrometry FluorescenceMESH: ImmunoblottingCell DeathMESH: Guidelines as Topic//purl.org/becyt/ford/3.1 [https]Bioquímica y Biología MolecularFlow Cytometry3. Good healthTunelMedicina Básicamedicine.anatomical_structureEukaryotic Cellscaspases030220 oncology & carcinogenesis//purl.org/becyt/ford/3 [https]MESH: Spectrometry FluorescenceMESH : Microscopy Electron ScanningProgrammed cell deathautophagyCIENCIAS MÉDICAS Y DE LA SALUDMESH: Microscopy Electron ScanningMESH : Flow CytometrycaspaseImmunoblottingGuidelines as TopicComputational biologyBiologyElectronFluorescenceArticle03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyModel organismddc:612mitotic catastropheMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Guidelines as Topic030304 developmental biologycell death; Apoptosis; caspase; autophagy; Oxidative stress; fluorescence microscopyMESH: Humansved/biologySpectrometryInterpretation (philosophy)MESH: ApoptosisMESH : Eukaryotic CellsMESH : HumansApoptosis; Eukaryotic Cells; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence; Cell Death; Molecular Biology; Cell Biologyimmunofluorescence microscopyCell BiologySpectrometry FluorescenceMicroscopy FluorescenceOxidative stressMESH : Cell DeathCancer cellMicroscopy Electron ScanningMESH : Apoptosis
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TRPC1 is regulated by caveolin-1 and is involved in oxidized LDL-induced apoptosis of vascular smooth muscle cells.

2009

International audience; Oxidized low-density lipoprotein (oxLDL) induced-apoptosis of vascular cells may participate in plaque instability and rupture. We have previously shown that vascular smooth muscle cells (VSMC) stably expressing caveolin-1 were more susceptible to oxLDL-induced apoptosis than VSMC expressing lower level of caveolin-1, and this was correlated with enhanced Ca(2+) entry and pro-apoptotic events. In this study, we aimed to identify the molecular events involved in oxLDL-induced Ca(2+) influx and their regulation by the structural protein caveolin-1. In VSMC, transient receptor potential canonical-1 (TRPC1) silencing by ARN interference prevents the Ca(2+) influx and red…

MESH: Lipoproteins LDLVascular smooth muscleOxysterolCaveolin 1ApoptosisBiologyMESH: Base SequenceMESH : RNA Small InterferingMuscle Smooth VascularTRPC1Transient receptor potential channelMESH: RNA Small InterferingMESH : Cells CulturedHumansMESH: Caveolin 1RNA Small InterferingMESH: TRPC Cation ChannelsCells CulturedTRPC Cation ChannelsMESH: HumansBase SequenceMESH : Gene Expression RegulationMESH: ApoptosisMESH : HumansMESH : TRPC Cation ChannelsMESH : Muscle Smooth VascularArticlesCell BiologyMESH: Muscle Smooth VascularActin cytoskeletonMESH: Gene Expression RegulationCell biologyLipoproteins LDLGene Expression RegulationApoptosisCaveolin 1MESH : Caveolin 1Molecular Medicinelipids (amino acids peptides and proteins)MESH : Base SequenceMESH : Lipoproteins LDLHomeostasisMESH : ApoptosisMESH: Cells Cultured
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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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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
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Long-Term Calorie Restriction Enhances Cellular Quality-Control Processes in Human Skeletal Muscle

2015

Calorie restriction (CR) retards aging, acts as a hormetic intervention, and increases serum corticosterone and HSP70 expression in rodents. However, less is known regarding the effects of CR on these factors in humans. Serum cortisol and molecular chaperones and autophagic proteins were measured in the skeletal muscle of subjects on CR diets for 3-15 years and in control volunteers. Serum cortisol was higher in the CR group than in age-matched sedentary and endurance athlete groups (15.6 ± 4.6 ng/dl versus 12.3 ± 3.9 ng/dl and 11.2 ± 2.7 ng/dl, respectively; p ≤ 0.001). HSP70, Grp78, beclin-1, and LC3 mRNA and/or protein levels were higher in the skeletal muscle of the CR group compared to…

Male0301 basic medicineGenetics and Molecular Biology (all)Time FactorsHydrocortisoneBiochemistryCortisolBody Mass IndexCluster Analysislcsh:QH301-705.5Endoplasmic Reticulum Chaperone BiPAldosteroneHeat-Shock ProteinsHSP70Serum cortisolMiddle Agedmedicine.anatomical_structureBeclin-1Femalemedicine.symptomMicrotubule-Associated Proteinsmedicine.drugAdultmedicine.medical_specialtyCalorie restrictionInflammationBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesEndurance trainingInternal medicineHeat shock proteinmedicineAutophagyHumansHSP70 Heat-Shock ProteinsRNA MessengerMuscle SkeletalExerciseCalorie restrictionCaloric RestrictionHydrocortisoneHSP70; aldosterone; autophagy; calorie restriction; cortisol; adult; apoptosis regulatory proteins; beclin-1; body mass index; cluster analysis; exercise; female; gene expression regulation; hsp70 heat-shock proteins; heat-shock proteins; humans; hydrocortisone; male; membrane proteins; microtubule-associated proteins; middle aged; muscle skeletal; RNA messenger; time factors; transcription factors; caloric restrictionCalorie restriction (CR)AutophagyMembrane ProteinsSkeletal muscleHsp70030104 developmental biologyEndocrinologylcsh:Biology (General)Gene Expression RegulationAldosterone; Autophagy; Calorie restriction; Cortisol; HSP70; Biochemistry Genetics and Molecular Biology (all)Apoptosis Regulatory ProteinsTranscription Factors
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Involvement of Bax and Bcl-2 in induction of apoptosis by essential oils of three Lebanese Salvia species in human prostate cancer cells

2018

Prostate cancer is one of the most common forms of cancer in men, and research to find more effective and less toxic drugs has become necessary. In the frame of our ongoing program on traditionally used Salvia species from the Mediterranean Area, here we report the biological activities of Salvia aurea, S. judaica and S. viscosa essential oils against human prostate cancer cells (DU-145). The cell viability was measured by 3(4,5-dimethyl-thiazol-2-yl)2,5-diphenyl-tetrazolium bromide (MTT) test and lactate dehydrogenase (LDH) release was used to quantify necrosis cell death. Genomic DNA, caspase-3 activity, expression of cleaved caspase-9, B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X (Ba…

Male0301 basic medicineSalvia miltiorrhiza<i>Salvia</i>; essential oil; prostate cancer; apoptosis; reactive oxygen specieslcsh:ChemistryProstate cancer0302 clinical medicineSalvialcsh:QH301-705.5Spectroscopybcl-2-Associated X Proteinreactive oxygen speciesCamphanesapoptosisGeneral Medicineprostate cancerComputer Science ApplicationsGene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisApoptosis Essential oil Prostate cancer Reactive oxygen species SalviaProgrammed cell deathSalvia; apoptosis; essential oil; prostate cancer; reactive oxygen speciesPanax notoginsengDNA FragmentationBiologyArticleCatalysisessential oilInorganic Chemistry03 medical and health sciencesBcl-2-associated X proteinCell Line TumorOils VolatilemedicineHumansViability assayPhysical and Theoretical ChemistryMolecular BiologyCell ProliferationCell growthOrganic ChemistryProstatic NeoplasmsCancerSettore CHIM/06 - Chimica Organicamedicine.diseaseapoptosi030104 developmental biologylcsh:Biology (General)lcsh:QD1-999ApoptosisCancer cellCancer researchbiology.proteinDrugs Chinese Herbal
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Polymorphisms of Pro-Inflammatory IL-6 and IL-1β Cytokines in Ascending Aortic Aneurysms as Genetic Modifiers and Predictive and Prognostic Biomarkers

2021

Background: Previous studies have demonstrated that polymorphisms involved in immune genes can affect the risk, pathogenesis, and outcome of thoracic ascending aortic aneurysms (TAAA). Here, we explored the potential associations of five functional promoter polymorphisms in interleukin-6 (IL-6), IL-1B, IL-1A, IL-18, and Tumor necrosis factor (TNF)A genes with TAAA. Methods: 144 TAAA patients and 150 age/gender matched controls were typed using KASPar assays. Effects on telomere length and levels of TAAA related histopathological and serological markers were analyzed. Results: Significant associations with TAAA risk were obtained for IL-6 rs1800795G&gt

Male0301 basic medicinemedicine.medical_specialtyInterleukin-1betamedial cell apoptosisSingle-nucleotide polymorphism030204 cardiovascular system & hematologyrs16944MicrobiologyPolymorphism Single NucleotideBiochemistryGastroenterologyArticleProinflammatory cytokinePathogenesis03 medical and health sciences0302 clinical medicineAneurysmInternal medicineGenotypeelastic fragmentationmedicinetelomere lengthHumansInterleukin 6thoracic ascending aortic aneurysmsMolecular BiologyAgedAortic Aneurysm ThoracicbiologyInterleukin-6business.industryMMP9Prognosismedicine.diseasers1800795QR1-502Settore MED/23030104 developmental biologyproinflammatory cytokinescystic medial changesbiology.proteinCytokinesBiomarker (medicine)FemaleTumor necrosis factor alphaInflammation MediatorsbusinessBiomarkersBiomolecules
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