Search results for "Apoptosis Regulator"

showing 10 items of 86 documents

Apoptosis resistance in epithelial tumors is mediated by tumor-cell-derived interleukin-4

2008

We investigated the mechanisms involved in the resistance to cell death observed in epithelial cancers. Here, we identify that primary epithelial cancer cells from colon, breast and lung carcinomas express high levels of the antiapoptotic proteins PED, cFLIP, Bcl-xL and Bcl-2. These cancer cells produced interleukin-4 (IL-4), which amplified the expression levels of these antiapoptotic proteins and prevented cell death induced upon exposure to TRAIL or other drug agents. IL-4 blockade resulted in a significant decrease in the growth rate of epithelial cancer cells and sensitized them, both in vitro and in vivo, to apoptosis induction by TRAIL and chemotherapy via downregulation of the antia…

AdultMaleProgrammed cell deathLung NeoplasmsTime Factorsapoptosis interleukin-4 cancer stem cells cancer chemiotherapy cytokinesCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinAntineoplastic AgentsApoptosisBreast NeoplasmsBiologyTNF-Related Apoptosis-Inducing LigandTumor Cells CulturedmedicineHumansAutocrine signallingMolecular BiologyInterleukin 4AgedCell ProliferationSettore MED/04 - Patologia GeneraleCell DeathDose-Response Relationship DrugCell growthCarcinomaIntracellular Signaling Peptides and ProteinsAntibodies MonoclonalInterleukin-4 Receptor alpha SubunitCorrectionCancerCell BiologyMiddle AgedPhosphoproteinsmedicine.diseaseUp-RegulationCell biologyAutocrine CommunicationProto-Oncogene Proteins c-bcl-2Drug Resistance NeoplasmApoptosisColonic NeoplasmsCancer cellFemaleInterleukin-4Interleukin-4 Cancer stem cellsSignal transductionApoptosis Regulatory ProteinsSignal Transduction
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DNA replication arrest in response to genotoxic stress provokes early activation of stress-activated protein kinases (SAPK/JNK).

2009

Abstract The impact of DNA damage-induced replication blockage for early activation of stress kinases [stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK)] is largely unknown. Here, we show that induction of dual phosphorylation of SAPK/JNK by the DNA polymerase inhibitor aphidicolin was not ameliorated by additional exposure to ultraviolet (UV) light, indicating that overlapping mechanisms participate in signaling to SAPK/JNK triggered by both agents. UV-induced DNA replication blockage, cyclobutane pyrimidine dimer formation and DNA strand break induction coincided with SAPK/JNK phosphorylation at early (≤ 30 min) but not late (≥ 2 h) time points after exposure. Genotoxin…

AphidicolinDNA ReplicationDNA damageUltraviolet RaysPoly ADP ribose polymeraseCell Linechemistry.chemical_compoundMiceAphidicolinStructural BiologyCricetinaeAnimalsHumansLymphocytesPhosphorylationProtein kinase AMolecular BiologyNucleic Acid Synthesis InhibitorsBRCA2 ProteinMice KnockoutbiologyKinaseCell CycleDNA replicationJNK Mitogen-Activated Protein KinasesFibroblastsMolecular biologyProliferating cell nuclear antigenDNA-Binding ProteinsEnzyme ActivationchemistryPyrimidine Dimersbiology.proteinPhosphorylationApoptosis Regulatory ProteinsDNA DamageJournal of molecular biology
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Induction of annexin-1 during TRAIL-induced apoptosis in thyroid carcinoma cells

2005

We investigated the expression of annexin-1 (ANXA1) in thyroid carcinoma cell lines and in thyroid cancers with a different degree of differentiation. The highest level of ANXA1 expression examined by Western blotting was detected in the papillary carcinoma cells (NPA) and in the follicular cells (WRO). On the other hand, the most undifferentiated thyroid carcinoma cells (ARO and FRO) presented the lowest level of ANXA1 expression. In surgical tissue specimens from 32 patients with thyroid cancers, we found high immunoreactivity for ANXA1 in papillary (PTC) and follicular (FTC) thyroid cancers while in undifferentiated thyroid cancers (UTC) the expression of the protein was barely detectabl…

ApoptosisTNF-Related Apoptosis-Inducing LigandApoptosis Regulatory ProteinsthyroidThyroid carcinomaTNF-Related Apoptosis-Inducing LigandText miningAnnexinMedicineHumansThyroid NeoplasmsMolecular BiologyThyroid NeoplasmAnnexin A1Apoptosis Regulatory ProteinMembrane Glycoproteinsbusiness.industryTumor Necrosis Factor-alphaApoptosiCell BiologyApoptosisCancer researchMembrane GlycoproteinbusinessApoptosis Regulatory ProteinsHuman
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Pharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothal…

2015

Endocannabinoids participate in the control of neurogenesis, neural cell death and gliosis. The pharmacological effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597, which limits the endocannabinoid degradation, was investigated in the present study. Cell proliferation (phospho-H3(+) or BrdU(+) cells) of the main adult neurogenic zones as well as apoptosis (cleaved caspase-3(+)), astroglia (GFAP(+)), and microglia (Iba1(+) cells) were analyzed in the hippocampus, hypothalamus and striatum of rats intraperitoneally treated with URB597 (0.3 mg/kg/day) at one dose/4-days resting or 5 doses (1 dose/day). Repeated URB597 treatment increased the plasma levels of the N-acylethanolamine…

AstrocitosNeurobiologia del desenvolupamentAmidohidrolasasCannabinoid receptorCarbamatos:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Intracellular Signaling Peptides and Proteins::Apoptosis Regulatory Proteins::Caspases [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Differentiation::Neurogenesis [Medical Subject Headings]medicine.medical_treatment:Chemicals and Drugs::Carbohydrates::Monosaccharides::Hexoses::Glucose [Medical Subject Headings]Apoptosis:Phenomena and Processes::Physiological Phenomena::Body Constitution::Body Weights and Measures::Body Size::Body Weight [Medical Subject Headings]chemistry.chemical_compound:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Membrane Proteins::Receptors Cell Surface::Receptors G-Protein-Coupled::Receptors Cannabinoid::Receptor Cannabinoid CB1 [Medical Subject Headings]0302 clinical medicine:Chemicals and Drugs::Organic Chemicals::Carboxylic Acids::Acids Acyclic::Carbamates [Medical Subject Headings]Fatty acid amide hydrolaseReceptor cannabinoide CB1:Organisms::Eukaryota::Animals [Medical Subject Headings]FAAHGliosishealth care economics and organizations:Chemicals and Drugs::Nucleic Acids Nucleotides and Nucleosides::Nucleosides::Deoxyribonucleosides::Deoxyuridine::Bromodeoxyuridine [Medical Subject Headings]:Chemicals and Drugs::Lipids::Glycerides::Triglycerides [Medical Subject Headings]Original Research0303 health sciencesNeurogenesisBenzamidas:Chemicals and Drugs::Polycyclic Compounds::Steroids::Cholestanes::Cholestenes::Cholesterol [Medical Subject Headings]Endocannabinoid systemEtanolaminas3. Good healthEndocannabinoides:Chemicals and Drugs::Lipids::Fatty Acids::Fatty Acids Unsaturated::Fatty Acids Monounsaturated::Oleic Acids [Medical Subject Headings]CannabinoidesMicroglíalipids (amino acids peptides and proteins)medicine.symptomColesterol:Chemicals and Drugs::Organic Chemicals::Hydrocarbons::Terpenes::Cannabinoids [Medical Subject Headings]:Chemicals and Drugs::Lipids::Fatty Acids::Palmitic Acids [Medical Subject Headings]psychological phenomena and processesProliferación celularmedicine.medical_specialtyCerebroNeurogenesiseducationBiologyBromodesoxiuridina:Anatomy::Nervous System::Neuroglia::Microglia [Medical Subject Headings]Triglicéridoslcsh:RC321-571Ácidos oléicosRatas03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineHipocampomedicineCaspasa 3:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hippocampus [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry030304 developmental biologyPalmitoylethanolamide:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Neurotransmitter Agents::Endocannabinoids [Medical Subject Headings]:Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Amidohydrolases [Medical Subject Headings]Cannabinoids:Anatomy::Cells::Neuroglia::Astrocytes [Medical Subject Headings]Peso corporalEnergy metabolism:Anatomy::Nervous System::Central Nervous System::Brain [Medical Subject Headings]:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hypothalamus [Medical Subject Headings]URB597:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death [Medical Subject Headings]:Diseases::Pathological Conditions Signs and Symptoms::Pathologic Processes::Gliosis [Medical Subject Headings]:Chemicals and Drugs::Organic Chemicals::Amines::Amino Alcohols::Ethanolamines [Medical Subject Headings]Muerte celular:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings]EndocrinologyURB597chemistryGliosisnervous systemGlucosaCannabinoidEnergy Metabolism:Chemicals and Drugs::Organic Chemicals::Amides::Benzamides [Medical Subject Headings]HipotálamoÁcidos palmíticos030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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Involvement of PAR-4 in Cannabinoid-Dependent Sensitization of Osteosarcoma Cells to TRAIL-Induced Apoptosis

2014

The synthetic cannabinoid WIN 55,212-2 is a potent cannabinoid receptor agonist with anticancer potential. Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells. Results show that WIN induced G2/M cell cycle arrest, which was associated with the induction of the main markers of ER stress (GRP78, CHOP and TRB3). In treated cells we also observed the conversion of the cytosolic form of the autophagosome marker LC3-I into LC3-II (the lipidated form located on the autophagosome membrane) and the enhanced incorporation of monodansylcadaverine and acridine orange, two markers of t…

AutophagosomeautophagyProgrammed cell deathCannabinoids ER stress autophagy TRAIL osteosarcoma cells GRP78/PAR-4 complex.Cannabinoid receptorMorpholinesCellApoptosisTRAILNaphthalenesBiologyGRP78/PAR-4 complex.Applied Microbiology and BiotechnologyTNF-Related Apoptosis-Inducing LigandCadaverineCell Line TumorSettore BIO/10 - BiochimicamedicineHumansRNA Small InterferingEndoplasmic Reticulum Chaperone BiPMolecular BiologyHeat-Shock ProteinsEcology Evolution Behavior and SystematicsCell ProliferationCannabinoid Receptor AgonistsOsteosarcomaCannabinoidsAutophagyCell Cycle Checkpointsosteosarcoma cellsCell BiologyCell cycleEndoplasmic Reticulum StressAcridine OrangeBenzoxazinesCell biologymedicine.anatomical_structureApoptosisAutophagosome membraneApoptosis Regulatory ProteinsER stressMicrotubule-Associated ProteinsResearch PaperDevelopmental Biology
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Protein quality control during aging involves recruitment of the macroautophagy pathway by BAG3.

2009

The Hsc/Hsp70 co-chaperones of the BAG (Bcl-2-associated athanogene) protein family are modulators of protein quality control. We examined the specific roles of BAG1 and BAG3 in protein degradation during the aging process. We show that BAG1 and BAG3 regulate proteasomal and macroautophagic pathways, respectively, for the degradation of polyubiquitinated proteins. Moreover, using models of cellular aging, we find that a switch from BAG1 to BAG3 determines that aged cells use more intensively the macroautophagic system for turnover of polyubiquitinated proteins. This increased macroautophagic flux is regulated by BAG3 in concert with the ubiquitin-binding protein p62/SQSTM1. The BAG3/BAG1 ra…

BAG domainProteasome Endopeptidase ComplexProtein familyProtein degradationBAG3ubiquitinationGeneral Biochemistry Genetics and Molecular BiologyBAG1ArticleRats Sprague-DawleyMiceUbiquitinMicroscopy Electron TransmissionAutophagyAnimalsHumansSQSTM1Molecular BiologyCellular SenescenceAdaptor Proteins Signal TransducingBAG1General Immunology and MicrobiologybiologyGeneral Neurosciencep62ImmunohistochemistryCell biologyRatsDNA-Binding ProteinsproteasomeProteasomeBiochemistrybiology.proteinApoptosis Regulatory ProteinsFlux (metabolism)Transcription FactorsThe EMBO journal
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Homozygous deletions localize novel tumor suppressor genes in B-cell lymphomas

2007

AbstractIntegrative genomic and gene-expression analyses have identified amplified oncogenes in B-cell non-Hodgkin lymphoma (B-NHL), but the capability of such technologies to localize tumor suppressor genes within homozygous deletions remains unexplored. Array-based comparative genomic hybridization (CGH) and gene-expression microarray analysis of 48 cell lines derived from patients with different B-NHLs delineated 20 homozygous deletions at 7 chromosome areas, all of which contained tumor suppressor gene targets. Further investigation revealed that only a fraction of primary biopsies presented inactivation of these genes by point mutation or intragenic deletion, but instead some of them w…

BiopsyDNA Mutational AnalysisGene DosageVesicular Transport ProteinsApoptosisBiochemistryEpigenesis Geneticimmune system diseaseshemic and lymphatic diseasesChromosomes HumanGenes Tumor SuppressorPromoter Regions GeneticSorting NexinsOligonucleotide Array Sequence AnalysisSequence DeletionBcl-2-Like Protein 11HomozygoteChromosome MappingNuclear ProteinsNucleic Acid HybridizationRNA-Binding ProteinsHematologyDNA NeoplasmBCL10Gene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2DNA methylationLymphoma B-CellTumor suppressor geneImmunologyBiologyGene dosageCell Line TumorProto-Oncogene ProteinsmedicineCyclin-Dependent Kinase Inhibitor p18HumansPoint MutationGene SilencingB cellAdaptor Proteins Signal TransducingHomeodomain ProteinsMembrane ProteinsCell BiologyDNA Methylationmedicine.diseaseMolecular biologyLymphomaCancer researchMantle cell lymphomaApoptosis Regulatory ProteinsCarrier ProteinsDiffuse large B-cell lymphomaTranscription Factors
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The Programmed Death (PD)‐1/PD‐Ligand 1 Pathway Regulates Graft‐Versus‐Host‐Reactive CD8 T Cells After Liver Transplantation

2008

Acute graft-versus-host disease (aGVHD) is a life-threatening complication after solid-organ transplantation, which is mediated by host-reactive donor T cells emigrating from the allograft. We report on two liver transplant recipients who developed an almost complete donor chimerism in peripheral blood and bone marrow-infiltrating T cells during aGVHD. By analyzing these T cells directly ex vivo, we found that they died by apoptosis over time without evidence of rejection by host T cells. The host-versus-donor reactivity was selectively impaired, as anti-third-party and antiviral T cells were still detectable in the host repertoire. These findings support the acquired donor-specific allotol…

CD4-Positive T-LymphocytesMaleCell TransplantationProgrammed Cell Death 1 ReceptorGraft vs Host DiseaseCD8-Positive T-LymphocytesTCIRG1MiceInterleukin 21Immune systemAntigenAntigens CDAnimalsHumansImmunology and AllergyCytotoxic T cellMedicinePharmacology (medical)IL-2 receptorMice KnockoutTransplantationbusiness.industryInterleukin-2 Receptor alpha SubunitForkhead Transcription FactorsMiddle AgedLiver TransplantationTransplantationsurgical procedures operativeGene Expression RegulationAntigens SurfaceImmunologyInterleukin 12Apoptosis Regulatory ProteinsbusinessImmunosuppressive AgentsAmerican Journal of Transplantation
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SAHA induces apoptosis in hepatoma cells and synergistically interacts with the proteasome inhibitor Bortezomib.

2007

Histone deacetylase (HDAC) inhibitors represent a promising group of anticancer agents. This paper shows that the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) stimulated at 5-10 microM apoptosis in human hepatoma HepG2 and Huh6 cells, but was ineffective in primary human hepatocytes (PHH). In HepG2 cells SAHA induced the extrinsic apoptotic pathway, increasing the expression of both FasL and FasL receptor and causing the activation of caspase-8. Moreover, SAHA enhanced the level of Bim proteins, stimulated alternative splicing of the Bcl-X transcript with the expression of the proapoptotic Bcl-Xs isoform, induced degradation of Bid into the apoptotic factor t-Bid and dephosphorylat…

Cancer ResearchCarcinoma HepatocellularFas Ligand ProteinClinical BiochemistryPharmaceutical ScienceApoptosisHydroxamic AcidsFas ligandHistone DeacetylasesBortezomibCell Line TumormedicineHumansProtease InhibitorsProtein kinase BVorinostatHDAC inhibitors . HepG2 cells . PHH . Extrinsic and intrinsic apoptotic pathwaysbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialCaspase 8VorinostatbiologyChemistryBortezomibCytochrome cBiochemistry (medical)Cell BiologyBoronic AcidsHistone Deacetylase InhibitorsProteasomeApoptosisPyrazinesProteasome inhibitorbiology.proteinCancer researchApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
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Breast cancer genome-wide association studies: there is strength in numbers.

2012

Breast cancer (BC) is a heterogeneous disease that exhibits familial aggregation. Family linkage studies have identified high-penetrance genes, BRCA1, BRCA2, PTEN and TP53, that are responsible for inherited BC syndromes. Moreover, a combination of family-based and population-based approaches indicated that genes involved in DNA repair, such as CHEK2, ATM, BRIP and PALB2, are associated with moderate risk. Therefore, all of these known genes account for only 25% of the familial aggregation cases. Recently, genome wide association studies (GWAS) in BC revealed single nucleotide polymorphisms (SNPs) in five novel genes associated to susceptibility: TNRC9, FGFR2, MAP3K1, H19 and lymphocyte-spe…

Cancer ResearchMultifactorial InheritanceSettore MED/06 - Oncologia MedicaPALB2PopulationMAP Kinase Kinase Kinase 1Single-nucleotide polymorphismGenome-wide association studyBreast NeoplasmsBiologyPolymorphism Single NucleotideGenetic linkageGeneticsSNPHumansGenetic Predisposition to DiseaseReceptor Fibroblast Growth Factor Type 2educationMolecular BiologyGeneCHEK2Geneticsbreast cancer GWASeducation.field_of_studyMicrofilament ProteinsHigh Mobility Group ProteinsCancer researchTrans-ActivatorsFemaleApoptosis Regulatory ProteinsReceptors ProgesteroneGenome-Wide Association StudyOncogene
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