Search results for " APOPTOSIS"

showing 10 items of 372 documents

A novel copper compound, CuNV110, induces apoptosis in tumor cells by dissociation of the Hsp60- pro-caspase 3 complex

2015

The biological activity of CuNV1110, a novel copper chemical compound, has been recently studied on cancer cells and it has been showed that it reduces the cell viability, in a dose and time dependent manner, and induces cell apoptosis. In this study we evaluated the possible mechanisms by which CuNV1110 induces cell apoptosis. In particular we looked at its effects on Hsp60 levels and caspase 3 activation. We used an in vitro model of a pulmonary mucoepidermoid carcinoma (NCI-H292 cells). We found that CuNV1110 reduces the cell viability and induces cell apoptosis in a dose/time dependent manner. Then, we found that Hsp60 levels decrease with the increasing concentrations of CuNV110; by co…

Respiratory cells; pulmonary cancer; Hsp60; caspase 3; apoptosis.Respiratory cells pulmonary cancer Hsp60 caspase 3 apoptosis
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Heat Shock Protein-60 and Risk for Cardiovascular Disease

2011

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecularchaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60,the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotectivebut a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examplesof specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicatea pathogenic role for HSP60 but also its …

Riskanimal structuresChaperonin Heat shock protein-60 cardiomyocytes heart failure cardiovascular diseases atherosclerosisChaperonin heat shock protein 60 cardiomyocytes heart failure cardiovascular disease atherosclerosis apoptosis microRNAs (miRs) diabetes Atrial fibrillationApoptosischemical and pharmacologic phenomenaDiseaseBioinformaticsAutoimmune DiseasesPathogenesisHeat shock proteinAtrial FibrillationDrug DiscoveryExtracellularAnimalsHumansMyocytes CardiacHeart FailurePharmacologybiologyfungiChaperonin 60AtherosclerosisResponse to treatmentCardiovascular DiseasesReperfusion InjuryChaperone (protein)HypertensionImmunologybiology.proteinHSP60Stress conditionsBiomarkersCurrent Pharmaceutical Design
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Red wine extract prevents neuronal apoptosis in vitro and reduces mortality of transgenic mice.

2007

In this work, we have investigated the effects of nutritional antioxidants as antidegenerative agents on glutamate-induced apoptosis in primary cultures of cerebellar granule neurons (CGNs). Glutamate-induced apoptosis is also associated with intracellular [Ca(2+)]i overload, generation of reactive oxygen species (ROS), depression of cell energy metabolism, cytochrome c release, and increase in caspase-3 activity. Pretreatment (3 h) with red wine extract (5 microg/mL) and ascorbic acid (30 microM) blocks glutamate-induced apoptosis in CGNs. In vivo experiments carried out on transgenic mice expressing the human mutated Cu, Zn superoxide dismutase (SOD1) G93A (mSOD1(G93A)) show that mice fed…

SOD1Glutamic AcidApoptosisMice TransgenicWinePharmacologyBiologycerebellar granule cells • apoptosis • lyophilized red wine • ASL • mSOD1G93AGeneral Biochemistry Genetics and Molecular BiologyMiceSuperoxide Dismutase-1History and Philosophy of ScienceIn vivoAnimalsHumansCells Culturedchemistry.chemical_classificationWineNeuronsReactive oxygen speciesCaspase 3Superoxide DismutaseGeneral NeuroscienceCytochrome cCytochromes cAscorbic acidSurvival AnalysisNeuroprotective AgentschemistryBiochemistryApoptosisbiology.proteinCalciumReactive Oxygen SpeciesIntracellular
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Suppressor of cytokine signaling 3 sensitizes anaplastic thyroid cancer to standard chemotherapy

2009

We previously showed that cancer cells from papillary, follicular, and anaplastic thyroid carcinomas produce interleukin-4 and interleukin-10, which counteract the cytotoxic activity of conventional chemotherapy through the up-regulation of antiapoptotic molecules. Here, we identify Janus kinase/signal transducers and activators of transcription (STAT) and phosphatidyl inositol 3-kinase (PI3K)/AKT as the down-stream pathways through which these cytokines confer resistance to cell death in thyroid cancer. We found that the absence of suppressors of cytokine signaling (SOCS) molecules allows the propagation of the survival signaling. Exogenous expression of SOCS1, SOCS3, and SOCS5 in the high…

STAT3 Transcription FactorCancer ResearchCancer Research; OncologyDown-RegulationMice NudeSuppressor of Cytokine Signaling Proteinsthyroidcancer spheres cytokines apoptosis chemoterapyMicePhosphatidylinositol 3-KinasesSuppressor of Cytokine Signaling 1 ProteinMedicineAnimalsHumansSOCS3Thyroid NeoplasmsAnaplastic thyroid cancerPhosphorylationThyroid cancerPI3K/AKT/mTOR pathwayAgedSettore MED/04 - Patologia GeneraleJanus kinase 1business.industrySuppressor of cytokine signaling 1Settore BIO/16 - Anatomia UmanaGene Transfer TechniquesCancerJanus Kinase 1Middle Agedmedicine.diseaseXenograft Model Antitumor AssaysSettore MED/18 - Chirurgia GeneraleOncologyDrug Resistance NeoplasmSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer researchFemalebusinessJanus kinaseSTAT6 Transcription FactorProto-Oncogene Proteins c-akt
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Parthenolide sensitizes hepatocellular carcinoma cells to trail by inducing the expression of death receptors through inhibition of STAT3 activation

2011

This article shows that HepG2, Hep3B, and SK-Hep1 cells, three lines of human hepatocellular carcinoma (HCC) cells, are resistant to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Parthenolide, a sesquiterpene lactone found in European feverfew, has been shown to exert both anti-inflammatory and anti-cancer activities. This article demonstrates that co-treatment with parthenolide and TRAIL-induced apoptosis with synergistic interactions in the three lines of HCC cells. In order to explain these effects we ascertained that parthenolide increased either at protein or mRNA level the total content of death receptors TRAIL-R1 and -R2 as well as their surfac…

STAT3 Transcription FactorCarcinoma HepatocellularPhysiologyClinical BiochemistryCellDown-RegulationTRAILApoptosisPharmacologyParthenolideSTAT3TNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSettore BIO/10 - BiochimicamedicineHumansParthenolidePhosphorylationReceptorSTAT3CaspaseJanus KinasesbiologyLiver NeoplasmsProto-Oncogene Proteins c-mdm2Hep G2 CellsReceptors Death DomainCell BiologyapoptosiEnzyme ActivationGene Expression Regulation Neoplasticmedicine.anatomical_structurechemistryCell cultureApoptosisCaspasesbiology.proteinSTAT proteinDrug Screening Assays AntitumorTumor Suppressor Protein p53SesquiterpenesJournal of Cellular Physiology
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The antitumor activities of curcumin and its isoxazole analogue are not affected by multiple gene expression changes in an MDR model of the MCF-7 bre…

2007

We examined the effects of curcumin and of its isoxazole analogue MR 39 in the MCF-7 breast cancer cell line and in its multidrug-resistant (MDR) variant MCF-7R. In comparison with MCF-7, MCF-7R lacks estrogen receptor alpha (ERalpha) and overexpressess P-glycoprotein (P-gp), different IAPs (inhibitory of apoptosis proteins) and COX-2. Through analyses of the effects on cell proliferation, cycling and death, we have observed that the antitumor activity of curcumin and of the more potent (approximately two-fold) MR 39 is at least equal in the MDR cell line compared to the parental MCF-7. Similar results were observed also in an MDR variant of HL-60 leukemia. RT-PCR evaluations performed in M…

STAT3 Transcription FactorCurcuminGene ExpressionEstrogen receptorBreast NeoplasmsBiologyPharmacologycurcumin isoxazole derivative multidrug resistance P-glycoprotein estrogen receptor inhibitory of apoptosis proteinschemistry.chemical_compoundCell Line TumorGeneticsHumansskin and connective tissue diseasesCell ProliferationP-glycoproteinCell DeathCell growthCell CycleTranscription Factor RelAGeneral MedicineCell cycleAntineoplastic Agents PhytogenicDrug Resistance MultipleMultiple drug resistancechemistryMCF-7Drug Resistance Neoplasmbiology.proteinCurcuminFemaleEstrogen receptor alpha
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Caratterizzazione proteomica di una linea beta cellulare resistente all'effetto citochinico

2012

SUMO apoptosis beta cellule diabeteSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioSettore MED/13 - Endocrinologia
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Conjunctival Sac Fluid Contains Elevated Levels of Soluble TRAIL: Implications for the Anti-Tumoral Surveillance of the Anterior Surface of the Eye

2008

Little is known on the ability of different epithelia to release soluble TNF-related apoptosis-inducing ligand (TRAIL) and the relevance of TRAIL secretion by epithelial cells is still incompletely understood. On these bases, we have measured the concentration of soluble TRAIL by ELISA in the conjunctival sac fluid. It was the highest ever detected in a biological fluid (mean value of 26,800 pg/ml), being approximately 20-fold greater than that found in human saliva and >200-fold greater than that detected in human serum. On the other hand, osteoprotegerin, the soluble decoy receptor of TRAIL, was almost undetectable in the conjunctival sac fluid. Of note, the levels of soluble TRAIL measur…

SalivaConjunctivaPhysiologyConjunctival sac fluidClinical BiochemistryApoptosisTRAILIn Vitro TechniquesBiologySettore MED/42 - Igiene Generale E ApplicataPhotorefractive Keratectomycorneal ephiteliumFlow cytometryCorneaTNF-Related Apoptosis-Inducing LigandOsteoprotegerinCell Line TumorCorneamedicineHumansCorneal epitheliumcorneal epitheliummedicine.diagnostic_testEye NeoplasmsOsteoprotegerinEpithelial CellsCell BiologyMolecular biologyRecombinant ProteinsBody Fluidsmedicine.anatomical_structureSolubilityanti-tumoral surveillanceImmunologyConjunctival sacImmunohistochemistrytrail; conjunctival sac fluid; corneal ephitelium; anti-tumoral surveillance.Conjunctiva
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Strategie di difesa attivate in risposta a stress, in embrioni di Paracentrotus lividus

2012

Sea urchin embryos are able to activate different defense strategies against stress. This model system allows to investigate numerous phenomena in multipotent cells, which interact among themselves, in their natural position, bypassing the disadvantages of isolated cells, deprived of their normal network. Cadmium (Cd) treatment triggers the accumulation of metal in embryonic cells and the activation of defense systems depending on concentration and exposure time, through the synthesis of heat shock proteins and/or the initiation of apoptosis. Here we show that Paracentrotus lividus embryos exposed to subacute/sublethal concentrations of Cd adopt autophagy as an additional stratagem to safeg…

Sea Urchin embryos Cadmium autophagy apoptosis stressSettore BIO/06 - Anatomia Comparata E Citologia
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Developmental defects induced by gadolinium ions in sea urchin embryos of phylogenetically distant species

2015

Gadolinium (Gd) is nowadays an emergent environmental pollutant: it is a metal of the lanthanide series of the elements whose chelates are commonly employed as contrast agents for magnetic resonance imaging and subsequently released into the aquatic environment. Sea urchin embryos are highly sensitive to several kinds of stressors and able to activate different defense strategies. The aim of this study was to analyze the consequences of embryo exposure to sublethal Gd concentrations. We compared the effects of Gd on the development of four phylogenetically distant sea urchin species: two Mediterranean species, Paracentrotus lividus and Arbacia lixula, and two species living in the East coas…

Sea UrchinAutophagyApoptosisSettore BIO/06 - Anatomia Comparata E CitologiaSea Urchin; Develpment; Pollution; Autophagy; ApoptosisDevelpmentPollution
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