Search results for "caspase"

showing 10 items of 390 documents

Resistance to diverse apoptotic triggers in multidrug resistant HL60 cells and its possible relationship to the expression of P-glycoprotein, Fas and…

2002

We studied the human HL60 leukemia cell line and its multidrug resistant (MDR) variant HL60R. In contrast to the HL60, HL60R showed an inability to undergo apoptosis from doxorubicin (Dox) or other different stimuli, including cisplatin, Fas ligation and serum withdrawal. HL60R cells lost surface Fas expression, but we found no evidence that Fas/FasL mediates the apoptotic effects of Dox in HL60. P-glycoprotein (P-gp) did not seem to play a major role as a specific inhibitor of apoptosis. In fact, the P-gp inhibitor verapamil reversed only partially the resistance to Dox-induced apoptosis of the MDR cells. In addition, it did not modify the rate of apoptosis induced from the other stimuli i…

Cancer ResearchProgrammed cell deathTime FactorsChromosomal Proteins Non-HistoneSurvivinDown-RegulationAntineoplastic AgentsApoptosisHL-60 CellsNerve Tissue ProteinsBiologyInhibitor of apoptosisFas ligandInhibitor of Apoptosis ProteinsInhibitory Concentration 50SurvivinTumor Cells CulturedHumansATP Binding Cassette Transporter Subfamily B Member 1RNA Messengerfas ReceptorP-glycoproteinInhibitor of apoptosis domainCaspase 3Reverse Transcriptase Polymerase Chain ReactionProteinsFlow CytometryNeuronal Apoptosis-Inhibitory ProteinNeoplasm ProteinsCell biologyProto-Oncogene Proteins c-bcl-2OncologyDoxorubicinDrug Resistance NeoplasmApoptosisCaspasesbiology.proteinInsect ProteinsNAIPCisplatinMicrotubule-Associated ProteinsCancer Letters
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Smac induces cytochrome c release and apoptosis independently from Bax/Bcl-xL in a strictly caspase-3-dependent manner in human carcinoma cells

2004

The mitochondrial apoptosis pathway mediates cell death through the release of various pro-apoptotic factors including cytochrome c and Smac, the second mitochondrial activator of caspases, into the cytosol. Smac was shown previously to inhibit IAP proteins and to facilitate initiation of the caspase cascade upon cytochrome c release. To investigate Smac function during apoptosis and to explore Smac as an experimental cancer therapeutic, we constructed an expression system based on a single adenoviral vector containing Smac under control of the Tet-off system supplied in cis. Conditional expression of Smac induced apoptosis in human HCT116 and DU145 carcinoma cells regardless of the loss of…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsBcl-xLCaspase 3Cysteine Proteinase InhibitorsAdenoviridaeMitochondrial ProteinsBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedGeneticsHumansMolecular BiologyCaspasebcl-2-Associated X ProteinCaspase-9biologyCaspase 3Cytochrome cCarcinomaIntracellular Signaling Peptides and ProteinsCytochromes cCaspase InhibitorsCaspase 9Cell biologyEnzyme ActivationProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesMutationbiology.proteinCancer researchbiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsCarrier ProteinsOligopeptidesProtein Processing Post-TranslationalOncogene
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Midregion PTHrP regulates Rip1 and caspase expression in MDA-MB231 breast cancer cells.

2007

It was previously reported that the midregion PTHrP domain (38-94)-amide restrains growth and invasion "in vitro", causes striking toxicity and accelerates death of some breast cancer cell lines, the most responsive being MDA-MB231 whose tumorigenesis was also attenuated "in vivo". In addition, we have demonstrated that midregion PTHrP is imported in the nucleoplasm of cultured MDA-MB231 cells, and that "in vitro" it can bind chromatin of metaphase spread preparations and also an isolated 20-mer oligonucleotide, thereby appearing endowed with a putative transcription factor-like DNA-binding ability. Here, we examined whether PTHrP (38-94)-amide was able to modulate the expression of genes e…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsPTHrP Rip1 caspase breast cancer cellsmedicine.disease_causeTransfectionCell MovementCell Line TumorGene expressionmedicineTranscriptional regulationHumansNeoplasm InvasivenessSettore BIO/06 - Anatomia Comparata E Citologiaskin and connective tissue diseasesCaspaseCell ProliferationNucleoplasmbiologyJNK Mitogen-Activated Protein KinasesParathyroid Hormone-Related ProteinRNA-Binding ProteinsOligonucleotides AntisenseMolecular biologyPeptide FragmentsChromatinCell biologyNuclear Pore Complex ProteinsSettore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaOncologyApoptosisCaspasesbiology.proteinFemalebcl-Associated Death ProteinCarcinogenesisSignal TransductionBreast cancer research and treatment
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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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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 of pr…

Cancer ResearchStromal cellbiologyApoptosisCell growthbiology.proteinCaspase 5Cell morphologyMolecular BiologyMolecular biologyCaspaseProtein kinase CCollagen receptorMolecular Carcinogenesis
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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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Increased endocannabinoid levels reduce the development of precancerous lesions in the mouse colon

2007

Colorectal cancer is an increasingly important cause of death in Western countries. Endocannabinoids inhibit colorectal carcinoma cell proliferation in vitro. In this paper, we investigated the involvement of endocannabinoids on the formation of aberrant crypt foci (ACF, earliest preneoplastic lesions) in the colon mouse in vivo. ACF were induced by azoxymethane (AOM); fatty acid amide hydrolase (FAAH) and cannabinoid receptor messenger ribonucleic acid (mRNA) levels were analyzed by the quantitative reverse transcription polymerase chain reaction (RT-PCR); endocannabinoid levels were measured by liquid chromatography-mass spectrometry; caspase-3 and caspase-9 expressions were measured by W…

Cannabinoid receptormedicine.medical_treatment2-Arachidonoylglycerolpreneoplastic lesionsMass Spectrometrychemistry.chemical_compoundMice0302 clinical medicineFatty acid amide hydrolaseDrug DiscoveryFatty acid amide hydrolase (FAAH)Aberrant crypt fociGenetics(clinical)ReceptorReceptors CannabinoidGenetics (clinical)Medicine(all)0303 health sciencesCaspase 3Reverse Transcriptase Polymerase Chain ReactionEndocannabinoid systemCaspase 93. Good health2-arachidonoylglycerolColon cancer030220 oncology & carcinogenesisColonic NeoplasmsMolecular Medicinelipids (amino acids peptides and proteins)psychological phenomena and processesRapid CommunicationAberrant crypt focimedicine.medical_specialtyColonAzoxymethaneBiologydigestive systemAmidohydrolases03 medical and health sciencesInternal medicineCannabinoid Receptor ModulatorsmedicineAnimalsRNA MessengerCannabinoid receptors030304 developmental biologyAzoxymethaneendocannabinoiddigestive system diseasesEndocrinologychemistrynervous systemCancer researchCannabinoidcancer pharmacologyPrecancerous ConditionsEndocannabinoids
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