Search results for "BCL-2"

showing 10 items of 197 documents

Pyrrolotetrazinones deazaanalogues of temozolomide induce apoptosis in Jurkat cell line: involvement of tubulin polymerization inhibition.

2009

Pyrrolotetrazinones are a new class of azolotetrazinones endowed with a high, remarkable antiproliferative activity in human tumor cultured cells. They hold the deaza skeleton of the antitumor drug temozolomide, although preliminary investigations indicated a different mechanism of action. To understand their mechanism(s) of action along with their target at molecular level, four derivatives were selected on the basis of their activity on a panel of human tumor cell lines and they were investigated in depth in a T leukemia cell line (Jurkat). Flow cytometric analysis of cell cycle after treatment with pyrrolotetrazinones has demonstrated that they were able to induce an arrest of the cell c…

MaleCancer ResearchProgrammed cell deathCarcinoma HepatocellularCell SurvivalCellGene ExpressionAntineoplastic AgentsApoptosisPhosphatidylserinesBiologyToxicologyJurkat cellsMicrotubulesMicrotubule polymerizationJurkat CellsMiceTubulinCell Line TumormedicineTemozolomideAnimalsHumansPharmacology (medical)Cell Proliferationbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialMice Inbred BALB CCaspase 3Cell CycleCell MembraneCell cycleSettore CHIM/08 - Chimica FarmaceuticaTubulin ModulatorsCell biologyMitochondriaDacarbazinemedicine.anatomical_structureOncologyMechanism of actionBiochemistryProto-Oncogene Proteins c-bcl-2ApoptosisCell culturemedicine.symptomPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesPyrrolotetrazinoneCancer chemotherapy and pharmacology
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IL-4 protects tumor cells from anti-CD95 and chemotherapeutic agents via up-regulation of antiapoptotic proteins

2004

Abstract We recently proposed that Th1 and Th2 cytokines exert opposite effects on the pathogenesis and clinical outcome of organ-specific autoimmunity by altering the expression of genes involved in target cell survival. Because a Th2 response against tumors is associated with poor prognosis, we investigated the ability of IL-4 to protect tumor cells from death receptor- and chemotherapy-induced apoptosis. We found that IL-4 treatment significantly reduced CD95 (Fas/APO-1)- and chemotherapeutic drug-induced apoptosis in prostate, breast, and bladder tumor cell lines. Analysis of antiapoptotic protein expression revealed that IL-4 stimulation resulted in up-regulation of cellular (c) FLIP/F…

MaleINFILTRATING LYMPHOCYTESCell SurvivalImmunologyCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinAntineoplastic AgentsApoptosisBreast NeoplasmsCARCINOMA-CELLSBiologySIGNALING PATHWAYSDownregulation and upregulationCell Line TumorImmunology and AllergyHumansfas ReceptorNON-HODGKINS-LYMPHOMACANCER PATIENTSReceptorBCL-2 PROTEINInterleukin 4EtoposideIL-4 apoptosis cancer stem cellsSettore MED/04 - Patologia GeneraleCHRONIC LYMPHOCYTIC-LEUKEMIAIntracellular Signaling Peptides and ProteinsAntibodies MonoclonalProstatic NeoplasmsFas receptorRecombinant ProteinsCell biologyUp-RegulationProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureFlipCancer researchT-CELLSCamptothecinFemaleInterleukin-4FLICE-INHIBITORY PROTEINSignal transductionCarrier ProteinsRENAL-CELL
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Study of Proliferation and Apoptosis in Neuroblastoma. Their Relation with Other Prognostic Factors

2002

Abstract Background Our objective was to study the proliferation and apoptotic process in 111 cases of neuroblastoma (NB) and to seek their relationship with other prognostic factors and survival. Methods Immunohistochemistry following ABC peroxidase was carried out for PCNA, Ki-67, bcl-2, and p53 proteins. Apoptosis analysis was performed with in situ detection of chromosomal breakdown. Molecular detection of DNA ladders by electrophoresis and amplification of MYCN was studied with PCR and Southern blot. Statistical study was performed with Pearson χ 2 and Kruskal-Wallis tests and Cox regression. Results Our results indicate that proliferative factors PCNA and Ki-67 were correlated to each…

MaleIn situProgrammed cell deathTime FactorsMitosisApoptosisPolymerase Chain ReactionNeuroblastomachemistry.chemical_compoundProliferating Cell Nuclear AntigenNeuroblastomamedicineHumansChildSouthern blotbiologyInfant NewbornInfantCell DifferentiationDNAGeneral MedicinePrognosismedicine.diseaseImmunohistochemistryMolecular biologyProliferating cell nuclear antigenBlotting SouthernKi-67 AntigenProto-Oncogene Proteins c-bcl-2chemistryApoptosisChild PreschoolMultivariate Analysisbiology.proteinImmunohistochemistryFemaleTumor Suppressor Protein p53Cell DivisionDNAFollow-Up StudiesArchives of Medical Research
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The antibiotic erythromycin induces tolerance against transient global cerebral ischemia in rats (pharmacologic preconditioning).

2006

Background Cerebral ischemic tolerance can be induced by a variety of noxious stimuli, but no clinically applicable regimen for preconditioning has been described. Therefore, the authors tested the ability of a pharmacologic preconditioning strategy using the well-known macrolide antibiotic erythromycin to induce tolerance against transient global cerebral ischemia in vivo. They also investigated whether tolerance induction by erythromycin involves transcriptional and translational changes of cerebral B-cell leukemia/lymphoma-2 (bcl-2) expression. Methods Male Wistar rats were treated with erythromycin (25 mg/kg intramuscularly) or vehicle and subjected to 15 min of transient global cerebr…

MaleIschemiaHippocampusErythromycinPharmacologyNeuroprotectionHippocampusIn vivomedicineAnimalsRNA MessengerRats WistarIschemic PreconditioningAntibacterial agentNeuronsbusiness.industrymedicine.diseaseAnti-Bacterial AgentsErythromycinRatsTolerance inductionAnesthesiology and Pain MedicineProto-Oncogene Proteins c-bcl-2Ischemic Attack TransientImmunologyReperfusionIschemic preconditioningbusinessmedicine.drugAnesthesiology
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MALT1 is deregulated by both chromosomal translocation and amplification in B-cell non-Hodgkin lymphoma

2003

The MALT1 gene was identified through its involvement in t(11;18)(q21;q21), seen in 30% of cases of mucosa-associated lymphoid tissue (MALT) lymphoma. Here, we show that deregulated MALT1 expression may occur in B-cell non-Hodgkin lymphoma (B-NHL) of various histologic subtypes either through translocation to the immunoglobulin heavy chain (IGH) locus or by genomic amplification. First, 2 cases, one case of MALT lymphoma and another of aggressive marginal zone lymphoma (MZL) with t(14;18)(q32;q21), cytogenetically identical to the translocation involving BCL2, were shown by fluorescence in situ hybridization (FISH) to involve MALT1, which lies about 5 Mb centromeric of BCL2. Molecular cloni…

MaleLymphoma B-CellImmunologyBiologyBiochemistryTranslocation Geneticimmune system diseaseshemic and lymphatic diseasesGene duplicationmedicineHumansRNA NeoplasmAgedChromosomes Human Pair 14medicine.diagnostic_testGene Expression ProfilingGene AmplificationMALT lymphomaLymphoma B-Cell Marginal ZoneCell BiologyHematologyMiddle Agedmedicine.diseaseMolecular biologyGenes bcl-2Neoplasm ProteinsGene Expression Regulation NeoplasticGene expression profilingMALT1Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinCaspasesB-Cell Non-Hodgkin LymphomaImmunoglobulin heavy chainFemaleChromosomes Human Pair 18Comparative genomic hybridizationFluorescence in situ hybridizationBlood
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Acceleration of glutathione efflux and inhibition of gamma-glutamyltranspeptidase sensitize metastatic B16 melanoma cells to endothelium-induced cyto…

2005

Highly metastatic B16 melanoma (B16M)-F10 cells, as compared with the low metastatic B16M-F1 line, have higher GSH content and preferentially overexpress BCL-2. In addition to its anti-apoptotic properties, BCL-2 inhibits efflux of GSH from B16M-F10 cells and thereby may facilitate metastatic cell resistance against endothelium-induced oxidative/nitrosative stress. Thus, we investigated in B16M-F10 cells which molecular mechanisms channel GSH release and whether their modulation may influence metastatic activity. GSH efflux was abolished in multidrug resistance protein 1 knock-out (MRP-/-1) B16M-F10 transfected with the Bcl-2 gene or in MRP-/-1 B16M-F10 cells incubated with l-methionine, wh…

MaleMelanoma ExperimentalCystic Fibrosis Transmembrane Conductance RegulatorApoptosisBiochemistryOligodeoxyribonucleotides Antisensechemistry.chemical_compoundMiceCell AdhesionAnimalsEndotheliumNeoplasm MetastasisCytotoxicityCell adhesionMolecular BiologybiologyActivator (genetics)Cell BiologyGlutathioneTransfectiongamma-GlutamyltransferaseMolecular biologyGlutathioneCystic fibrosis transmembrane conductance regulatorMice Inbred C57BLKineticsOxidative StresschemistryProto-Oncogene Proteins c-bcl-2VerapamilApoptosisbiology.proteinEffluxMultidrug Resistance-Associated ProteinsThe Journal of biological chemistry
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Mitochondrial biogenesis fails in secondary biliary cirrhosis in rats leading to mitochondrial DNA depletion and deletions

2011

Chronic cholestasis is characterizedby mitochondrial dysfunction, associated with loss of mitochondrialmembrane potential, decreased activities of respiratory chaincomplexes, and ATP production. Our aim was to determine themolecular mechanisms that link long-term cholestasis to mitochondrialdysfunction. We studied a model of chronic cholestasis inducedby bile duct ligation in rats. Key sensors and regulators of theenergetic state and mitochondrial biogenesis, mitochondrial DNA(mtDNA)-to-nuclear DNA (nDNA) ratio (mtDNA/nDNA) relativecopy number, mtDNA deletions, and indexes of apoptosis (BAX,BCL-2, and cleaved caspase 3) and cell proliferation (PCNA) wereevaluated. Our results show that long…

MaleMitochondrial DNAPhysiologyMitochondrial TurnoverMitochondrial HepatopathyNF-E2-Related Factor 1Respiratory chainMitochondria LiverProtein Serine-Threonine KinasesMitochondrionBiologyDNA MitochondrialSirtuin 1CholestasisProliferating Cell Nuclear AntigenPhysiology (medical)medicineAnimalsRats Wistarbcl-2-Associated X ProteinCholestasisHepatologyCaspase 3Liver Cirrhosis BiliaryGastroenterologyPyruvate Dehydrogenase Acetyl-Transferring KinaseRNA-Binding ProteinsTFAMmedicine.diseaseGA-Binding Protein Transcription FactorPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMolecular biologyRatsGenes MitochondrialProto-Oncogene Proteins c-bcl-2Mitochondrial biogenesisChronic DiseaseBile DuctsGene DeletionTranscription FactorsAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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Immunohistochemical Expression of Ki-67 Antigen, Cox-2 and Bax/Bcl-2 in Prostate Cancer; Prognostic Value in Biopsies and Radical Prostatectomy Speci…

2005

Abstract Purposes: To elucidate the prognostic value of the immunohistochemical (IHC) expression of Bcl-2, Bax, Cox-2 and Ki-67 antigen in biopsy cores (C) and surgical specimens (SP) of prostate cancer (PC) and to determine the C to SP reproducibility. Material and methods: The IHC study was carried out in 91 patients operated by means of radical prostatectomy (RP) with available formalin-fixed paraffin-embedded material from both C and SP. Results: The IHC expression of Bcl-2 in C and SP was very low (5%). Bax was expressed in almost all the patients and did not show any prognostic value. We observed a good reproducibility between C and SP for all molecules except with Bax. In prostate C,…

MaleOncologymedicine.medical_specialtyPathologyBiopsyUrologymedicine.medical_treatmentDisease-Free SurvivalProstate cancerProstateInternal medicineBiopsyBiomarkers TumormedicineHumansAgedRetrospective Studiesbcl-2-Associated X ProteinProstatectomyUnivariate analysismedicine.diagnostic_testbiologyProstatectomybusiness.industryMembrane ProteinsProstatic NeoplasmsAnatomical pathologyMiddle AgedPrognosismedicine.diseaseImmunohistochemistryKi-67 Antigenmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Cyclooxygenase 2Ki-67Multivariate AnalysisDisease Progressionbiology.proteinImmunohistochemistrybusinessEuropean Urology
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Tolerance-Inducing Dose of 3-Nitropropionic Acid Modulates bcl-2 and bax Balance in the Rat Brain: A Potential Mechanism of Chemical Preconditioning

2000

Many studies have reported ischemia protection using various preconditioning techniques, including single dose 3-nitropropionic acid (3-NPA), a mitochondrial toxin. However, the cellular signal transduction cascades resulting in ischemic tolerance and the mechanisms involved in neuronal survival in the tolerant state still remain unclear. The current study investigated the mRNA and protein expression of the antiapoptotic bcl-2 and the proapoptotic bax, two antagonistic members of the bcl-2 gene family, in response to a single dose of 3-NPA, to global cerebral ischemia–reperfusion, and to the combination of both 3-NPA-pretreatment and subsequent global cerebral ischemia–reperfusion. Brain h…

MalePathologymedicine.medical_specialtyIschemiaPharmacologyBiology030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicineBcl-2-associated X proteinDrug toleranceProto-Oncogene ProteinsGene expressionmedicineAnimalsRNA MessengerRats WistarIschemic Preconditioningbcl-2-Associated X ProteinMessenger RNABrainDrug ToleranceNitro Compoundsmedicine.diseasePathophysiologyRatsReal-time polymerase chain reactionProto-Oncogene Proteins c-bcl-2NeurologyIschemic Attack TransientApoptosisbiology.proteinNeurology (clinical)PropionatesCardiology and Cardiovascular Medicine030217 neurology & neurosurgeryJournal of Cerebral Blood Flow & Metabolism
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Sodium metabisulfite as a cytotoxic food additive induces apoptosis in HFFF2 cells

2021

Sodium metabisulfite (SMB), an antioxidant agent, is extensively used as a preservative in food industry. The current study was aimed to clarify its potential toxic effects on human fetal foreskin fibroblasts (HFFF2) cells, in vitro. Subsequently, MTT results illustrated that exposure to SMB significantly (p  0.0001) decreased HFFF2 cell viability in a dose-dependent manner, and the concentration of 25 μM reduced cell survival rates to 50% as the half-maximal inhibitory concentration of SMB. It was further shown that SMB exerted this cytotoxic effect on HFFF2 cells through apoptosis induction. qRT-PCR and western blotting results showed that treatment of HFFF2 cells with this food additive …

MalePreservativeAntioxidantfood.ingredientCell Survivalmedicine.medical_treatmentForeskinApoptosisPharmacology01 natural sciencesAnalytical Chemistrychemistry.chemical_compound0404 agricultural biotechnologyfoodAutophagymedicineHumansSulfitesCytotoxic T cellCytotoxicityCells Culturedbcl-2-Associated X ProteinCaspase 8Dose-Response Relationship DrugCaspase 3Food additive010401 analytical chemistry04 agricultural and veterinary sciencesGeneral MedicineSodium metabisulfiteFibroblasts040401 food scienceCaspase 9In vitro0104 chemical sciencesGene Expression RegulationchemistryApoptosisFood AdditivesReactive Oxygen SpeciesFood ScienceFood Chemistry
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