Search results for " apoptosis."

showing 10 items of 359 documents

Sodium phenylbutyrate induces apoptosis in human retinoblastoma Y79 cells: The effect of combined treatment with the topoisomerase I-inhibitor topote…

2001

Our results demonstrate that sodium phenylbutyrate, a compound with a low degree of toxicity, exerted a cytotoxic effect on human retinoblastoma Y79 cells in a time- and dose-dependent manner. Treatment of Y79 cells for 72 h with phenylbutyrate reduced cell viability by 63% at 2 mM and 90% at 4 mM. Cell death caused by phenylbutyrate exhibited the typical features of apoptosis, as shown by light and fluorescent microscopy. Western blot analysis demonstrated that exposure of Y79 cells to phenylbutyrate decreased the level of the antiapoptotic factor Bcl-2 and induced the activation of caspase-3, a key enzyme in the execution phase of apoptosis. Moreover, treatment with phenylbutyrate markedl…

Cancer ResearchProgrammed cell deathCell SurvivalBlotting WesternApoptosisPhenylbutyrateHistonesSettore BIO/10 - BiochimicamedicineTumor Cells CulturedHumansretinoblastoma apoptosis sodium phenylbutirateViability assayEnzyme InhibitorsbiologyCaspase 3TopoisomeraseRetinoblastomaSodium phenylbutyrateAcetylationDrug SynergismCell cyclePhenylbutyrateseye diseasesEnzyme ActivationOncologyProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinCancer researchTopotecanDrug Therapy CombinationTopoisomerase I InhibitorsTumor Suppressor Protein p53Topotecanmedicine.drug
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Apoptosis and the liver

2000

Regulation of the homeostatic balance between cell proliferation and programmed cell death, apoptosis, is essential for development and maintenance of multicellular organisms. Apoptosis is a genetically and evolutionarily highly conserved process. Analysis of the molecular mechanisms of apoptosis has led to a better understanding of many human diseases. Notably in cancer, but also in infectious or autoimmune disease, a deficiency in apoptosis is one of the key events in pathophysiology. On the other hand, overefficient apoptosis, as observed in fulminant liver failure, may be equally harmful for the organism indicating that a tight regulation of the apoptotic machinery is essential for surv…

Cancer ResearchProgrammed cell deathCeramideHepatitis Viral HumanDNA damageCellGenes mycApoptosisBiologyReceptors Tumor Necrosis Factorchemistry.chemical_compoundmedicineHumansfas ReceptorLiver DiseasesLiver NeoplasmsIntrinsic apoptosisGenes p53Genes bcl-2Liver TransplantationCell biologymedicine.anatomical_structureLiverchemistryUVB-induced apoptosisApoptosisImmunologyPoly(ADP-ribose) PolymerasesSignal transductionReceptors Transforming Growth Factor betaSeminars in Cancer Biology
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SGK-1 protects kidney cells against apoptosis induced by ceramide and TNF-α

2015

AbstractCeramide regulates several different cellular responses including mechanisms leading to apoptosis. Serum- and glucocorticoid-inducible protein kinase (SGK)-1 is a serine threonine kinase, which activates survival pathways in response to stress stimuli. Recently, we demonstrated an anti-apoptotic role of SGK-1 in human umbilical endothelial cells treated with high glucose. In the present study, since ceramide induces apoptosis by multiple mechanisms in diabetes and its complication such as nephropathy, we aimed to investigate whether SGK-1 may protect even against apoptosis induced by ceramide in kidney cells. Human embryonic kidney (HEK)-293 cells stable transfected with SGK-1 wild …

Cancer ResearchProgrammed cell deathCeramideSettore MED/09 - Medicina InternaDIABETES MELLITUSImmunologyProtein Serine-Threonine KinasesTNF ALPHABiologyCeramidesKidneyTransfectionImmediate-Early ProteinsSettore MED/13 - EndocrinologiaCellular and Molecular Neurosciencechemistry.chemical_compoundHumansSettore MED/49 - Scienze Tecniche Dietetiche ApplicateProtein kinase ASettore MED/04 - Patologia GeneraleSerine/threonine-specific protein kinaseTumor Necrosis Factor-alphaCERAMIDEKinaseHEK 293 cellsKidney metabolismCell BiologyLipid signalingINSULINAPOPTOSIS3. Good healthCell biologyHEK293 CellschemistryINSULIN CERAMIDE DIABETES MELLITUS TNF ALPHA APOPTOSISOriginal ArticleCell Death & Disease
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Targeting apoptosis proteins in hematological malignancies

2010

The apoptotic machinery plays a key role in hematopoietic cell homeostasis. Terminally differentiated cells are eliminated, at least in part, by apoptosis, whereas part of the apoptotic machinery, including one or several caspases, is required to go through very specific steps of the differentiation pathways. A number of hematological diseases involve a deregulation of this machinery, which in most cases is a decrease in cell sensitivity to pro-apoptotic signals through over-expression of anti-apoptotic molecules. In some situations however, e.g. in the erythroid lineage of low grade myelodysplastic syndromes, cell sensitivity to apoptosis is increased in a death receptor-dependent manner a…

Cancer ResearchProgrammed cell deathFas Ligand ProteinMyeloidCellular differentiationAmino Acid MotifsAntineoplastic AgentsApoptosisLigandsInhibitor of apoptosisTNF-Related Apoptosis-Inducing LigandCell Line TumormedicineHumansReceptorCaspasebiologyIntrinsic apoptosisCell DifferentiationCell biologyGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyApoptosisHematologic Neoplasmsbiology.proteinDrug Screening Assays AntitumorApoptosis Regulatory ProteinsSignal TransductionCancer Letters
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Oligodendroglioma cells shed microvesicles which contain TRAIL as well as molecular chaperones and induce cell death in astrocytes.

2011

Microvesicles (MVs) shed from G26/24 oligodendroglioma cells were previously reported to cause a reproducible, dose-dependent, inhibitory effect on neurite outgrowth, and eventually neuronal apoptosis, when added to primary cultures of rat cortical neurons. These effects were reduced but not abolished by functional monoclonal antibodies against Fas-L. In order to investigate whether MVs contain other factors able to induce cell death, we tested them for TRAIL and found clear evidence of its presence in the vesicles. This finding suggests the possibility that Fas-L and TRAIL cooperate in inducing brain cell death. Aimed at understanding the route through which the vesicles deliver their mess…

Cancer ResearchProgrammed cell deathNeuritemedicine.drug_classOligodendrogliomaCellCell CommunicationBiologyMonoclonal antibodyTNF-Related Apoptosis-Inducing LigandCell-Derived MicroparticlesmedicineAnimalsHSP70 Heat-Shock ProteinsRats WistarCells CulturedCell DeathVesicleHSC70 Heat-Shock ProteinsCell cycleMicrovesiclesRatsCell biologymedicine.anatomical_structureOncologyApoptosisAstrocytesCulture Media Conditionedmicrovesicles oligodendroglioma astrocytes TRAIL Hsp70Molecular Chaperones
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Dynamic survivin in head and neck cancer: Molecular mechanism and therapeutic potential

2007

Although disease management of head and neck squamous cell carcinomas (HNSCC) has improved significantly, therapy resistance leading to tumor recurrence still counteracts improvement of long-term survival. Consequently, identification of molecular markers that signal increased risk of treatment failure or, which can be exploited by targeted therapy, is urgently needed. Survivin is strongly expressed in HNSCC, and its proposed dual role as an apoptosis inhibitor and a mitotic effector positioned survivin in the front line of cancer research. Notably, survivin is detected as a cytoplasmic and as a nuclear protein in HNSCC patients, which stimulated numerous studies to investigate and to specu…

Cancer ResearchProgrammed cell deathPathologymedicine.medical_specialtyApoptosis InhibitorSurvivinmedicine.medical_treatmentCellBiologyInhibitor of Apoptosis ProteinsTargeted therapySurvivinBiomarkers TumormedicineAnimalsHumansNuclear proteinneoplasmsHead and neck cancerCell cyclePrognosismedicine.diseaseNeoplasm Proteinsmedicine.anatomical_structureOncologyHead and Neck NeoplasmsCancer researchMicrotubule-Associated ProteinsBiologie
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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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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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MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts

2013

The oncogenes MYCN and survivin (BIRC5) maintain aggressiveness of diverse cancers including sarcomas. To investigate whether these oncogenes cooperate in initial malignant transformation, we transduced them into Rat-1 fibroblasts. Indeed, survivin enhanced MYCN-driven contact-uninhibited and anchorage-independent growth in vitro. Importantly, upon subcutaneous transplantation into mice, cells overexpressing both instead of either one of the oncogenes generated tumors with shortened latency, marked anaplasia and an increased proliferation-to-apoptosis ratio resulting in accelerated growth. Mechanistically, the increased tumorigenicity was associated with an enhanced Warburg effect and a hyp…

Cancer ResearchSurvivinBlotting WesternApoptosisBiologyReal-Time Polymerase Chain ReactionN-Myc Proto-Oncogene ProteinInhibitor of Apoptosis ProteinsMalignant transformationImmunoenzyme TechniquesMiceAdenosine TriphosphateSurvivinmedicineAnimalsHumansLactic AcidRNA MessengerneoplasmsAnaplasiaCells CulturedCell ProliferationHomeodomain ProteinsOncogene ProteinsN-Myc Proto-Oncogene ProteinReverse Transcriptase Polymerase Chain ReactionCell growthNuclear ProteinsGeneral MedicineFibroblastsWarburg effectCell HypoxiaRatsTransplantationCell Transformation NeoplasticGlucoseHypoxia-inducible factorsCancer researchmedicine.symptomGlycolysisCarcinogenesis
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MUC1 oncoprotein promotes refractoriness to chemotherapy in thyroid cancer cells.

2007

Abstract Overexpression of MUC1 oncoprotein is frequently observed in cancer and contributes to confer resistance to genotoxic agents. Papillary, follicular, and anaplastic thyroid carcinomas are the three forms of thyroid epithelial cancer. Anaplastic tumors are less differentiated and extremely aggressive, characterized by a poor prognosis. Little is known about the role of MUC1 in thyroid cancer. We recently showed that autocrine production of interleukin (IL)-4 and IL-10 controls thyroid cancer cell survival, growth, and resistance to chemotherapy through activation of Janus-activated kinase/signal transducers and activators of transcription (JAK/STAT) and phosphatidylinositide 3′-OH ki…

Cancer ResearchTranscription GeneticDrug ResistanceApoptosisSuppressor of Cytokine Signaling ProteinsnPhosphatidylinositol 3-KinasesAntibioticsMedicineRNA Small InterferingThyroid cancerTumorAntibiotics AntineoplasticThyroidAntineoplasticInterleukin-10Mitochondriamedicine.anatomical_structureOncologyTranscriptionSignal TransductionDown-RegulationSmall InterferingTransfectionCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinGeneticSettore MED/04 - PATOLOGIA GENERALEAntigens NeoplasmCell Line TumorHumansThyroid NeoplasmsAnaplastic thyroid cancerAntigensProtein kinase BPI3K/AKT/mTOR pathwayAntibiotics Antineoplastic; Antigens Neoplasm; Apoptosis; Cell Line Tumor; Down-Regulation; Doxorubicin; Drug Resistance Neoplasm; Humans; Interleukin-10; Interleukin-4; Mitochondria; Mucin-1; Mucins; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; RNA Small Interfering; Signal Transduction; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Transcription Genetic; Transfection; Cancer Research; Oncologybusiness.industryMucin-1MucinsCancermedicine.diseaseDoxorubicinDrug Resistance NeoplasmCancer cellCancer researchNeoplasmRNAInterleukin-4businessProto-Oncogene Proteins c-aktCancer research
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