Search results for "Caspases"

showing 10 items of 157 documents

Sodium butyrate induces apoptosis in human hepatoma cells by a mitochondria/caspase pathway, associated with degradation of beta-catenin, pRb and Bcl…

2004

Butyrate can promote programmed cell death in a number of tumour cells in vitro. This paper provides evidence that butyrate induces apoptosis in human hepatoma HuH-6 and HepG2 cells but is ineffective in Chang liver cells, an immortalised non-tumour cell line. In both HuH-6 and HepG2 cells, apoptosis appeared after a lag period of approximately 16 h and increased rapidly during the second day of treatment. In particular, the effect was stronger in HuH-6 cells, which were, therefore, chosen for ascertaining the mechanism of butyrate action. In HuH-6 cells, beta-catenin seemed to exert an important protective role against apoptosis, since pretreatment with beta-catenin antisense ODN reduced t…

Cancer ResearchProgrammed cell deathbeta-CateninCarcinoma HepatocellularBlotting Westernbcl-X ProteinCaspase 3Bcl-xLApoptosisButyrateCell LineMembrane Potentialschemistry.chemical_compoundSettore BIO/10 - BiochimicaCyclin DCyclinsCyclin EHumansCaspasebeta CateninbiologyReverse Transcriptase Polymerase Chain ReactionCytochrome cLiver NeoplasmsSodium butyrateMolecular biologyButyratesCytoskeletal ProteinspRbOncologychemistryProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinTrans-ActivatorsPoly(ADP-ribose) PolymerasesEuropean journal of cancer (Oxford, England : 1990)
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The role of oxidative stress in apoptosis induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid in human colon adenocarcinoma …

2008

Histone deacetylase inhibitors (HDACIs) activate genes that promote cell cycle arrest and apoptosis in a number of tumor cells. This study showed that suberoylanilide hydroxamic acid (SAHA), a potent and commonly used HDACI, induced apoptosis in human colon adenocarcinoma HT-29 cells in a time- and dose-dependent manner. This effect was accompanied by the induction of oxidative stress, dissipation of mitochondrial transmembrane potential and activation of executioner caspases. Moreover, SAHA increased the levels of phosphorylated active forms of p38 and JNK. The addition of either the antioxidant N-acetylcysteine or the specific inhibitor of NADPH oxidase diphenylene iodonium chloride reduc…

Cancer ResearchProgrammed cell deathmedicine.drug_classCell Survivalp38 mitogen-activated protein kinasesBlotting WesternApoptosisAdenocarcinomamedicine.disease_causeHydroxamic AcidsAntioxidantsSettore BIO/10 - BiochimicamedicineHumansEnzyme InhibitorsProtein kinase BCaspaseMembrane Potential MitochondrialVorinostatbiologyHistone deacetylase inhibitorEnzyme ActivationHistone Deacetylase InhibitorsOxidative StressOncologyBiochemistryApoptosisCaspasesColonic NeoplasmsCancer researchbiology.proteinHistone deacetylaseReactive Oxygen Speciescolon adenomacarcinoma cells histone deacetylase inhibitors apoptosisHT29 CellsOxidative stressSignal TransductionInternational journal of oncology
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Ganciclovir-induced apoptosis in HSV-1 thymidine kinase expressing cells: critical role of DNA breaks, Bcl-2 decline and caspase-9 activation.

2002

Although ganciclovir (GCV) is most often used in suicide anticancer gene therapy, the mechanism of GCV-induced cell killing and apoptosis is not fully understood. We analysed the mechanism of apoptosis triggered by GCV using a model system of CHO cells stably transfected with HSV-1 thymidine kinase (HSVtk). GCV-induced apoptosis is due to incorporation of the drug into DNA resulting in replication-dependent formation of DNA double-strand breaks and, at later stages, S and G2/M arrest. GCV-provoked DNA instability was likely to be responsible for the observed initial decline in Bcl-2 level and caspase-9/-3 activation. Further decline in the Bcl-2 level was due to cleavage of the protein by c…

Cancer ResearchTime FactorsvirusesPoly ADP ribose polymeraseApoptosisCytochrome c GroupCHO CellsHerpesvirus 1 HumanTransfectionThymidine KinaseCricetinaeGeneticsAnimalsfas ReceptorMolecular BiologyGanciclovirbiologyReverse Transcriptase Polymerase Chain ReactionCytochrome cCell CycleTransfectionSuicide geneFas receptorMolecular biologyCaspase 9Enzyme ActivationGene Expression Regulation NeoplasticCell killingProto-Oncogene Proteins c-bcl-2ApoptosisThymidine kinaseCaspasesbiology.proteinPoly(ADP-ribose) PolymerasesDNA DamageOncogene
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Apoptosis: focus on sea urchin development

2009

It has been proposed that the apoptosis is an essential requirement for the evolution of all animals, in fact the apoptotic program is highly conserved from nematodes to mammals. Throughout development, apoptosis is employed by multicellular organisms to eliminate damaged or unnecessary cells. Here, we will discuss both developmental programmed cell death (PCD) under normal conditions and stress induced apoptosis, in sea urchin embryos. Sea urchin represent an excellent model system for studying embryogenesis and cellular processes involved in metamorphosis. PCD plays an essential role in sculpting and remodelling the embryos and larvae undergoing metamorphosis. Moreover, this marine organi…

Cancer Researchanimal structuresmedia_common.quotation_subjectClinical BiochemistryDefence mechanismsPharmaceutical ScienceApoptosisEmbryos PCD Stress CaspasesApoptosis evolution EchinodermsEvolution Molecularbiology.animalAnimalsSettore BIO/06 - Anatomia Comparata E CitologiaMetamorphosisSea urchinCaspasemedia_commonPharmacologybiologyEcologyBiochemistry (medical)EmbryogenesisEmbryoCell BiologyCell biologyMulticellular organismApoptosisSea Urchinsembryonic structuresbiology.proteinApoptosis
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Do not stress, just differentiate: role of stress proteins in hematopoiesis

2015

Hematopoiesis permits the constant regeneration of the blood system and is a permanent example of cell differentiation. Defects in its tight regulation can lead to either cell death or abnormal proliferation and may translate into multiple types of blood disorders, including leukemia. Heat shock proteins (HSPs), the expression of which is controlled by heat shock factors (HSFs, currently four known members),1 are a set of highly conserved proteins induced in response to a wide variety of physiological and environmental stress. HSP/HSF overexpression or mislocalization has been described in many cancers, particularly in hematology, and other diseases. Therefore, the involvement of HSFs/HSPs …

Cancer Researchmedicine.medical_specialtyCellular differentiationImmunologyBiologyMiceCellular and Molecular NeuroscienceHeat Shock Transcription FactorsInternal medicineHeat shock proteinmedicineAnimalsProtein IsoformsRNA MessengerHeat shockTranscription factorHeat-Shock ProteinsHematologyCell DifferentiationNews and CommentaryCell BiologyHematopoiesisCell biologyDNA-Binding ProteinsHeat shock factorHaematopoiesisCaspasesHSP60Heat-Shock ResponseTranscription FactorsCell Death & Disease
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Cigarette Smoke Extract Induces p38 MAPK-Initiated, Fas-Mediated Eryptosis

2022

Eryptosis is a physiological mechanism for the clearance of senescent or damaged erythrocytes by phagocytes. Excessive eryptosis is stimulated under several pathologies and associated with endothelial injury and thrombosis. Cigarette smoke (CS) is an established risk factor for vascular diseases and cigarette smokers have high-levels of eryptotic erythrocytes. This study, for the first time, investigates the mechanism by which CS damages red blood cells (RBCs). CS extract (CSE) from commercial cigarettes was prepared and standardized for nicotine content. Cytofluorimetric analysis demonstrated that treatment of human RBCs with CSE caused dose-dependent, phosphatidylserine externalization an…

Caspase 8ErythrocytesCaspase 3cigarette smokeOrganic ChemistryGeneral Medicinep38 MAPKCeramidesp38 Mitogen-Activated Protein KinasesCatalysisComputer Science ApplicationsInorganic Chemistryeryptosis; cigarette smoke; death-inducing signaling complex (DISC); p38 MAPK; ceramide; caspasescaspasesSmokeeryptosisSettore BIO/10 - BiochimicaTobaccodeath-inducing signaling complex (DISC)HumansceramidePhysical and Theoretical ChemistryReactive Oxygen SpeciesMolecular BiologySpectroscopy
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Type V collagen and protein kinase C η down-regulation in 8701-BC breast cancer cells.

2011

We previously reported that ductal infiltrating carcinomas (d.i.c.) of the human breast display profound modifications of the stromal architecture, associated with anomalous collagen composition. Among the major alterations observed in the interstitial collagen, the relative increase of type V collagen content was detected. When type V collagen was used as an ‘‘in vitro’’ substrate for 8701-BC d.i.c. cells, it appeared able to restrain cell growth, inhibit cell motility and invasion ‘‘in vitro’’, and modify the expression levels of genes coding for apoptosis factors, caspases and stress response proteins. In the present paper we demonstrate that type V collagen induces the down-regulation o…

Caspase 8bcl-X ProteinDown-RegulationApoptosisBreast NeoplasmsDNA FragmentationOligonucleotides AntisenseGene Expression Regulation NeoplasticIsoenzymesCaspasesCell Line TumorHumansFemalebcl-Associated Death ProteinSettore BIO/06 - Anatomia Comparata E CitologiaCollagen Type Vdifferential display protein kinase breast cancer gene expression collagenProtein Kinase CCell ProliferationMolecular carcinogenesis
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Induction of apoptosis by arachidonic acid in human retinoblastoma Y79 cells: involvement of oxidative stress

2000

Arachidonic acid administration caused apoptosis in Y79 cells, as shown by typical morphological changes, phosphatidylserine externalization, chromatin condensation, processing and activation of caspase-3 and cleavage of the endogenous caspase substrate poly-(ADP-ribose)-polymerase. Arachidonic acid also caused lamin B cleavage, suggesting caspase-6 activation. Arachidonic acid treatment was accompanied by increased formation of the lipid peroxidation end products malondialdehyde and 4-hydroxy-2-nonenal, lowering in reduced glutathione content and in mitochondrial membrane potential. Inhibiting glutathione synthesis sensitized Y79 cells to apoptosis-inducing stimuli, whilst replenishing red…

Cell SurvivalBlotting WesternApoptosisCell Countmedicine.disease_causeMembrane PotentialsLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundPhospholipase A2medicineTumor Cells Culturedarachidonic acidHumansCYP2C8biologyDose-Response Relationship DrugRetinoblastomaGlutathioneTrypan BlueMalondialdehydeFlow CytometryGlutathioneSensory SystemsCell biologyMitochondriaOphthalmologyOxidative StressBiochemistrychemistryMitochondrial permeability transition poreCaspasesbiology.proteinArachidonic acidColorimetryPoly(ADP-ribose) PolymerasesOxidative stress
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Powerful tumor cell growth-inhibiting activity of a synthetic derivative of atractyligenin: Involvement of PI3K/Akt pathway and thioredoxin system

2014

The semi-synthetic ent-kaurane 15-ketoatractyligenin methyl ester (SC2017) has been previously reported to possess high antiproliferative activity against several solid tumor-derived cell lines. Our study was aimed at investigating SC2017 tumor growth-inhibiting activity and the underlying mechanisms in Jurkat cells (T-cell leukemia) and xenograft tumor models. METHODS: Cell viability was evaluated by MTT assay. Cell cycle progression, reactive oxygen species (ROS) elevation and apoptotic hallmarks were monitored by flow cytometry. Inhibition of thioredoxin reductase (TrxR) by biochemical assays. Levels and/or activation status of signaling proteins were assessed by western blotting. Xenogr…

CellBiophysicsAntineoplastic AgentsApoptosisAtractylosideBiologyCell cycleBiochemistryJurkat cellsMicePhosphatidylinositol 3-KinasesThioredoxinsTumor Cells CulturedmedicineAnimalsHumansMTT assayViability assaySettore BIO/15 - Biologia FarmaceuticaMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationPI3K/AktHCT 116 xenograftCytochromes cApoptosiThioredoxin systemSettore CHIM/06 - Chimica OrganicaCell cycleXenograft Model Antitumor AssaysCell biologymedicine.anatomical_structureCaspasesCancer researchThioredoxinDiterpenes KauraneProto-Oncogene Proteins c-aktEnt-kaurane
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Anandamide-induced apoptosis in Chang liver cells involves ceramide and JNK/AP-1 pathway

2006

In the present study we demonstrate that anandamide, the most important endogenous cannabinoid, markedly induced apoptosis in Chang liver cells, an immortalized non-tumor cell line derived from normal liver tissue, while it induced only modest effects in a number of hepatoma cell lines. The apoptotic effect was reduced by methyl-beta-cyclodextrin, a membrane cholesterol depletor, suggesting an interaction between anandamide and the membrane microdomains named lipid rafts. Anandamide effects were mediated by the production of ceramide, as demonstrated by experiments performed with the sphingomyelinase inhibitor, desipramine, or with the sphingomyelinase activator, melittin. This conclusion w…

CeramideProgrammed cell deathFas Ligand ProteinCell SurvivalPolyunsaturated AlkamidesLiver cytologyp38 mitogen-activated protein kinasesBlotting WesternApoptosisArachidonic AcidsBiologyCeramidesCell LineMembrane Potentialschemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsGeneticsHumansEnzyme InhibitorsMembrane GlycoproteinsBcl-2-Like Protein 11Dose-Response Relationship DrugDesipramineJNK Mitogen-Activated Protein KinasesMembrane ProteinsFree Radical ScavengersGeneral MedicineAnandamideEndocannabinoid systemAcetylcysteineCell biologyEnzyme ActivationTranscription Factor AP-1cannabinoids apoptosis tumor cells JNK/AP1LiverchemistryApoptosisCaspasesMitochondrial MembranesTumor Necrosis FactorsApoptosis Regulatory ProteinsSphingomyelinEndocannabinoidsSignal TransductionInternational Journal of Molecular Medicine
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