Search results for "Apoptotic Signaling"

showing 6 items of 6 documents

Geldanamycin-induced osteosarcoma cell death is associated with hyperacetylation and loss of mitochondrial pool of heat shock protein 60 (hsp60)

2013

Osteosarcoma is one of the most malignant tumors of childhood and adolescence that is often resistant to standard chemo- and radio-therapy. Geldanamycin and geldanamycin analogs have been recently studied as potential anticancer agents for osteosarcoma treatment. Here, for the first time, we have presented novel anticancer mechanisms of geldanamycin biological activity. Moreover, we demonstrated an association between the effects of geldanamycin on the major heat shock proteins (HSPs) and the overall survival of highly metastatic human osteosarcoma 143B cells. We demonstrated that the treatment of 143B cells with geldanamycin caused a subsequent upregulation of cytoplasmic Hsp90 and Hsp70 w…

Cell SurvivalLactams Macrocycliclcsh:MedicineApoptosisBone NeoplasmsBiologyMitochondrionMitochondrial Proteinschemistry.chemical_compoundGeldanamycin Hsp60 Osteosarcoma cellHeat shock proteinCell Line Tumorpolycyclic compoundsBenzoquinonesHumansHeat shocklcsh:ScienceCell ProliferationOsteosarcomaMultidisciplinaryAntibiotics Antineoplasticlcsh:RAcetylationChaperonin 60GeldanamycinHsp90Molecular biologyMitochondriaProtein TransportchemistryCancer cellCancer researchbiology.proteinApoptotic signaling pathwayHSP60lcsh:QDrug Screening Assays AntitumorProtein Processing Post-TranslationalResearch ArticleSignal Transduction
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Galectin-3 Impairment of MYCN-Dependent Apoptosis-Sensitive Phenotype Is Antagonized by Nutlin-3 in Neuroblastoma Cells

2012

MYCN amplification occurs in about 20-25% of human neuroblastomas and characterizes the majority of the high-risk cases, which display less than 50% prolonged survival rate despite intense multimodal treatment. Somehow paradoxically, MYCN also sensitizes neuroblastoma cells to apoptosis, understanding the molecular mechanisms of which might be relevant for the therapy of MYCN amplified neuroblastoma. We recently reported that the apoptosis-sensitive phenotype induced by MYCN is linked to stabilization of p53 and its proapoptotic kinase HIPK2. In MYCN primed neuroblastoma cells, further activation of both HIPK2 and p53 by Nutlin-3 leads to massive apoptosis in vitro and to tumor shrinkage an…

Galectin 3Cancer TreatmentGene Dosagelcsh:MedicineApoptosisProtein-Serine-Threonine KinaseBiochemistryPiperazineschemistry.chemical_compoundNeuroblastoma0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchSignaling in Cellular Processeslcsh:ScienceEnergy-Producing OrganellesApoptotic SignalingNuclear ProteinOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinMultidisciplinaryCell DeathImidazolesOncogene ProteinNuclear ProteinsTransfectionNutlin3. Good healthGene Expression Regulation NeoplasticProtein TransportCell killingPhenotypeOncologyGalectin-3030220 oncology & carcinogenesisGene Knockdown TechniquesMedicineResearch ArticleSignal TransductionHumanBiologyBioenergeticsProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinModels Biological03 medical and health sciencesNeuroblastomaCell Line TumormedicineHumansBiologyImidazolePiperazineneoplasms030304 developmental biologylcsh:RGene AmplificationChemotherapy and Drug Treatmentmedicine.diseasechemistryCell cultureApoptosisPediatric OncologyCytoprotectionGene Knockdown TechniqueCancer researchlcsh:QTumor Suppressor Protein p53Carrier ProteinsCarrier ProteinDNA Damage
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Pterostilbene-induced tumor cytotoxicity: a lysosomal membrane permeabilization-dependent mechanism.

2012

The phenolic phytoalexin resveratrol is well known for its health-promoting and anticancer properties. Its potential benefits are, however, limited due to its low bioavailability. Pterostilbene, a natural dimethoxylated analog of resveratrol, presents higher anticancer activity than resveratrol. The mechanisms by which this polyphenol acts against cancer cells are, however, unclear. Here, we show that pterostilbene effectively inhibits cancer cell growth and stimulates apoptosis and autophagosome accumulation in cancer cells of various origins. However, these mechanisms are not determinant in cell demise. Pterostilbene promotes cancer cell death via a mechanism involving lysosomal membrane …

PterostilbeneCancer Treatmentlcsh:MedicineApoptosisResveratrolBiochemistryLung and Intrathoracic Tumorschemistry.chemical_compoundMolecular cell biologyRNA interferenceNeoplasmsPhagosomesStilbenesDrug DiscoveryBreast TumorsBasic Cancer Researchlcsh:ScienceCytotoxicitySkin TumorsApoptotic Signaling CascadeCellular Stress ResponsesMultidisciplinaryMicroscopy ConfocalCell DeathMalignant MelanomaFlow CytometryCellular StructuresSignaling CascadesCell biologyEukaryotic CellsOncologyCaspasesMedicineCellular TypesCell DivisionResearch ArticleSignal TransductionProgrammed cell deathDrugs and DevicesDrug Research and DevelopmentMitosisAntineoplastic AgentsBiologyPermeabilityCell GrowthInhibitory Concentration 50NecrosisComplementary and Alternative MedicineCell Line TumorGastrointestinal TumorsAutophagyHumansHSP70 Heat-Shock ProteinsBiologyCell ProliferationDose-Response Relationship DrugL-Lactate DehydrogenaseCell growthlcsh:RAutophagyProteinsCancers and NeoplasmsRegulatory ProteinschemistrySubcellular OrganellesApoptosisResveratrolCancer celllcsh:QGene expressionLysosomesCytometryPloS one
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Caspase-3 contributes to ZO-1 and Cl-5 tight-junction disruption in rapid anoxic neurovascular unit damage.

2011

BACKGROUND: Tight-junction (TJ) protein degradation is a decisive step in hypoxic blood-brain barrier (BBB) breakdown in stroke. In this study we elucidated the impact of acute cerebral ischemia on TJ protein arrangement and the role of the apoptotic effector protease caspase-3 in this context. METHODOLOGY/PRINCIPAL FINDINGS: We used an in vitro model of the neurovascular unit and the guinea pig whole brain preparation to analyze with immunohistochemical methods the BBB properties and neurovascular integrity. In both methodological approaches we observed rapid TJ protein disruptions after 30 min of oxygen and glucose deprivation or middle cerebral artery occlusion, which were accompanied by…

Time FactorsAnatomy and Physiologylcsh:MedicineMiceMolecular Cell BiologyPathologySignaling in Cellular ProcessesHypoxia Brainlcsh:ScienceCells CulturedNeuropathologyApoptotic SignalingMultidisciplinaryTight junctionCaspase 3ChemistryAnimal ModelsCell biologyTransport proteinProtein Transportmedicine.anatomical_structureNeurologyBlood-Brain BarrierMedicineResearch ArticleSignal TransductionClinical Research DesignCerebrovascular DiseasesGuinea PigsIschemiaContext (language use)Caspase 3Protein degradationBlood–brain barrierNeurological SystemTight JunctionsCapillary PermeabilityModel OrganismsDiagnostic MedicinemedicineAnimalsTransient Ischemic AttacksAnimal Models of DiseaseClaudinBiologyIschemic Strokelcsh:REndothelial CellsMembrane ProteinsPhosphoproteinsmedicine.diseaseAnatomical PathologyClaudinsImmunologyZonula Occludens-1 ProteinNervous System Componentslcsh:QPLoS ONE
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Triclosan induces Fas receptor-dependent apoptosis in mouse neocortical neurons in vitro

2014

Triclosan (TCS) is a commonly used antimicrobial agent in personal care and sanitizing products, as well as in household items. Numerous studies have demonstrated the presence of TCS in various human tissues. Several studies have reported the accumulation of TCS in fish and human brain tissue. The aim of the present study was to investigate the effect of TCS on apoptosis in mouse neocortical neurons after 7 days of culture in vitro following 3, 6 and 24 h of exposure. To explore the mechanism underlying the effects of TCS in neurons, we studied the activation and protein expression of the Fas receptor (FasR) and caspase- 8, caspase-9 and caspase-3, as well as DNA fragmentation in TCS-treate…

Time FactorsExtrinsic apoptotic signaling pathwayApoptosisNeocortexDNA fragmentation.DNA FragmentationCaspase 8caspase-8FasRMicePregnancyAnimalsfas ReceptorFADDEnzyme InhibitorsCells CulturedNeuronsDose-Response Relationship DrugL-Lactate DehydrogenasebiologyGeneral NeurosciencefungiEmbryo MammalianStaurosporineFas receptorApoptotic bodyTriclosanIn vitroCell biologyBiochemistryApoptosisCaspasesbiology.proteinFatty Acid Synthesis InhibitorsDNA fragmentationFemaleNeuroscience
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Plexin-B1 activates NF-κB and IL-8 to promote a pro-angiogenic response in endothelial cells.

2011

Background The semaphorins and their receptors, the plexins, are proteins related to c-Met and the scatter factors that have been implicated in an expanding signal transduction network involving co-receptors, RhoA and Ras activation and deactivation, and phosphorylation events. Our previous work has demonstrated that Semaphorin 4D (Sema4D) acts through its receptor, Plexin-B1, on endothelial cells to promote angiogenesis in a RhoA and Akt-dependent manner. Since NF-κB has been linked to promotion of angiogenesis and can be activated by Akt in some contexts, we wanted to examine NF-κB in Sema4D treated cells to determine if there was biological significance for the pro-angiogenic phenotype o…

animal structuresRHOAProto-Oncogene Proteins c-aktAngiogenesisSignaling in cellular processesG-protein signalingCancer TreatmentSEMA4Dlcsh:MedicineSignal transductionBiology03 medical and health sciencesMolecular cell biology0302 clinical medicineSemaphorinSettore BIO/10 - BiochimicaAkt Signaling CascadeMembrane Receptor SignalingInterleukin 8lcsh:ScienceBiologyProtein kinase BGTPase signalingRas signaling030304 developmental biology0303 health sciencesMultidisciplinaryMechanisms of Signal Transductionlcsh:RSignaling Cascades3. Good healthCell biologyPlexin B1RNA interferencepro-angiogenicendothelial cellsOncology030220 oncology & carcinogenesisembryonic structuresCancer researchbiology.proteinMedicinelcsh:QAntiangiogenesis TherapyAntiapoptotic signalingSignal transductionResearch ArticlePLoS ONE
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