Search results for " APOPTOSIS"

showing 10 items of 372 documents

Acute organ failure following the loss of anti-apoptotic cellular FLICE-inhibitory protein involves activation of innate immune receptors

2014

Apoptosis signaling is involved in both physiological tissue homeostasis and acute and chronic diseases. The role of regulatory apoptosis signaling molecules and their organ-specific functions are less defined. Therefore, we investigated the loss of the anti-apoptotic cellular FLICE-inhibitory protein (cFLIP) and the mechanisms of the resulting lethal organ failure in vivo using inducible knockout mice. These were generated by crossing floxed cFLIP mice to a tamoxifen inducible Rosa26-creERT2 mouse strain. Death following global loss of cFLIP resulted from liver failure, accumulation of M1-polarized macrophages and accompanying hepatic cell death and inflammation. Apoptosis was also promine…

Programmed cell deathCASP8 and FADD-Like Apoptosis Regulating ProteinMice TransgenicInflammationBiologyMiceImmune systemmedicineAnimalsMolecular BiologyTissue homeostasisOriginal PaperInnate immune systemMacrophagesMembrane ProteinsCell BiologyLiver Failure AcuteImmunity InnateCell biologyToll-Like Receptor 4TransplantationApoptosisToll-Like Receptor 9Stimulator of interferon genesHepatocytesmedicine.symptomCell Death & Differentiation
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The abrogation of the HOXB7/PBX2 complex induces apoptosis in melanoma through the miR-221&222-c-FOS pathway.

2013

Cutaneous melanoma is the fastest increasing cancer worldwide. Although several molecular abnormalities have been associated with melanoma progression, the underlying mechanisms are still largely unknown and few targeted therapies are under evaluation. Here we show that the HOXB7/PBX2 dimer acts as a positive transcriptional regulator of the oncogenic microRNA-221 and -222. In addition, demonstrating c-FOS as a direct target of miR-221&222, we identify a HOXB7/PBX2→miR-221&222 →c-FOS regulatory link, whereby the abrogation of functional HOXB7/PBX2 dimers leads to reduced miR-221&222 transcription and elevated c-FOS expression with consequent cell death. Taking advantage of the treatment wit…

Programmed cell deathCancer ResearchSkin NeoplasmsTranscription GeneticApoptosisSmall Interferingc-FosPolymerase Chain ReactionCell LineGeneticCell Line TumorProto-Oncogene ProteinsHOXB7/PBX2 complexmicroRNATranscriptional regulationmedicinemelanomaHumansPBXRNA Small InterferingDNA PrimersHomeodomain Proteinsc-FOS pathwayTumorbiologymicroRNABase SequenceMelanomaHOXB7; HXR9 peptide; melanoma; microRNA; PBX; Apoptosis; Base Sequence; Cell Line Tumor; DNA Primers; Dimerization; Homeodomain Proteins; Humans; Melanoma; MicroRNAs; Polymerase Chain Reaction; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-fos; RNA Small Interfering; Skin Neoplasms; Transcription Genetic; Cancer Research; Oncologymedicine.diseaseMicroRNAsHXR9 peptideOncologyApoptosisCell cultureCutaneous melanomaHOXB7/PBX2 complex ;melanoma ;c-FOS pathwayCancer researchbiology.proteinHOXB7RNATranscriptionDimerizationProto-Oncogene Proteins c-fosCancer Cell Biology
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Antitumor effects of dehydroxymethylepoxyquinomicin, a novel nuclear factor-kappaB inhibitor, in human liver cancer cells are mediated through a reac…

2009

Activation of the nuclear transcription factor-kappa B (NF-kappa B) has been implicated in liver tumorigenesis. We evaluated the effects of a novel NF-kappa B inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), in two human liver cancer cell lines HA22T/VGH and HuH-6. DHMEQ treatment dose dependently decreased the DNA-binding capacity of the NF-kappa B p65 subunit, inhibited cell growth and proliferation, and increased apoptosis as shown by caspase activation, release of cytochrome c, poly(ADP-ribose) polymerase cleavage, and down-regulation of survivin. DHMEQ also induced a dose-dependent activation of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling, …

Programmed cell deathCarcinoma HepatocellularBIOLOGICAL-ACTIVITIESDrug Evaluation PreclinicalDown-RegulationAntineoplastic AgentsApoptosisBiologymedicine.disease_causeACTIVATIONchemistry.chemical_compoundHYDROGEN-PEROXIDEENDOPLASMIC-RETICULUM STRESSCell Line TumorSurvivinNADPH OXIDASEmedicineHumansOXIDATIVE STRESSProtein kinase AEndoplasmic Reticulum Chaperone BiPINDUCED APOPTOSISCell ProliferationPharmacologySettore MED/12 - GastroenterologiaDose-Response Relationship DrugUNFOLDED PROTEIN RESPONSECell growthCyclohexanonesINDUCTIONLiver NeoplasmsDEATHNF-kappa BCytochromes cMolecular biologyCell biologyEnzyme ActivationchemistryApoptosisCaspasesCancer cellBenzamidesSettore BIO/14 - FarmacologiaMolecular MedicineGrowth inhibitionMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesOxidative stressMolecular pharmacology
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Poriferan survivin exhibits a conserved regulatory role in the interconnected pathways of cell cycle and apoptosis

2010

Survivin orchestrates intracellular pathways during cell division and apoptosis. Its central function as mitotic regulator and inhibitor of cell death has major implications for tumor cell proliferation. Analyses in early-branching Metazoa so far propose an exclusive role of survivin as a chromosomal passenger protein, whereas only later during evolution a complementary antiapoptotic function might have arisen, concurrent with increased organismal complexity. To lift the veil on the ancestral function(s) of this key regulator, a survivin-like protein (SURVL) of one of the earliest-branching metazoan taxa was identified and functionally characterized. SURVL of the sponge Suberites domuncula …

Programmed cell deathCell divisionRecombinant Fusion ProteinsMolecular Sequence DataApoptosisTransfectionCell LineInhibitor of Apoptosis ProteinsLipopeptidesSurvivinAnimalsHumansAmino Acid SequenceMolecular BiologyMitosisGeneticsOriginal PaperBase SequencebiologyCell CycleCell BiologyCell cyclebiology.organism_classificationCell biologySuberites domunculaCell cultureCaspasesSuberitesSequence AlignmentCell DivisionIntracellularCadmiumCell Death & Differentiation
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Short-term exposure to cadmium affects the expression of stress response and apoptosis-related genes in immortalized epithelial cells from the human …

2009

Abstract It is known that cadmium (Cd) evokes cell responses that not only involve protective reactions against toxicity but also induces cell death. Increasing interest has been recently focused on the elucidation of the cellular and molecular aspects of Cd-dependent regulation of gene expression in different model systems. Here, we examined the effects of short-term (24 h) exposure of immortalized non-tumoral HB2 cells from human breast epithelium to CdCl2 at 50 μM concentration, corresponding to the IC50 for this time of incubation. The possible occurrence of apoptosis-related events was evaluated via analysis of the physical state of the DNA and of the membrane localization of phosphaty…

Programmed cell deathCellApoptosisPhosphatidylserinesBiologyToxicologyCell LineInhibitory Concentration 50Heat shock proteinGene expressionmedicineHumansSettore BIO/06 - Anatomia Comparata E CitologiaGeneRegulation of gene expressionCell DeathCell MembraneEpithelial CellsDNAGeneral MedicineCell biologyGene Expression Regulation Neoplasticmedicine.anatomical_structurecadmium gene expression apoptosis stress response epithelial cellsCell cultureApoptosisFemaleCadmiumToxicology in Vitro
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GD3 ganglioside directly targets mitochondria in a bcl-2-controlled fashion.

2000

Lipid and glycolipid diffusible mediators are involved in the intracellular progression and amplification of apoptotic signals. GD3 ganglioside is rapidly synthesized from accumulated ceramide after the clustering of death-inducing receptors and triggers apoptosis. Here we show that GD3 induces dissipation of DeltaPsim and swelling of isolated mitochondria, which results in the mitochondrial release of cytochrome c, apoptosis inducing factor, and caspase 9. Soluble factors released from GD3-treated mitochondria are sufficient to trigger DNA fragmentation in isolated nuclei. All these effects can be blocked by cyclosporin A, suggesting that GD3 is acting at the level of the permeability tran…

Programmed cell deathCeramideApoptosisMitochondria LiverMitochondrionliverBiochemistryMembrane Potentialschemistry.chemical_compoundGangliosidesGeneticsAnimalsMolecular BiologySettore MED/04 - Patologia GeneralebiologyCytochrome cCaspase 9SialyltransferasesCell biologyRatsmitochondriaEnzyme ActivationchemistryMitochondrial permeability transition poreProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinCyclosporinecaspases; cyclosporine; proto-oncogene proteins c-bcl-2; sialyltransferases; caspase 9; rats; animals; enzyme activation; apoptosis; membrane potentials; gangliosides; mitochondria liver; subcellular fractionsApoptosis-inducing factorlipids (amino acids peptides and proteins)ApoptosomeBiotechnologySubcellular FractionsFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Insulin and IGFs induce apoptosis in chick embryo retinas deprived of L-glutamine

1999

In chick embryo retinas, cultured in serum-free medium lacking L-glutamine, IGF-I, IGF-II and insulin induced apoptotic DNA fragmentation and cell death, IGF-I being the most efficacious compound. The apoptotic effect, which was particularly evident in retinas removed from 7-day-old chick embryos, declined with the age of the embryos and disappeared after day 11. Apoptosis appeared after a time lag of 8 h and then increased with time up to 16 h. Cycloheximide, an inhibitor of protein synthesis, was capable of entirely abolishing apoptotic cell death. The effect induced by IGFs or insulin was suppressed by the addition of glutamine. Cytokine-mediated apoptosis was also observed after withdra…

Programmed cell deathChemistryInsulinmedicine.medical_treatmentApoptotic DNA fragmentationEmbryoRetinalCell BiologyAnatomyCycloheximideCell biologyGlutaminechemistry.chemical_compoundApoptosismedicineInsulin apoptosis chick embryo retina development growth factorsMolecular Biology
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Novel ways to sensitise gastrointestinal cancer to apoptosis.

2009

Gastrointestinal (GI) cancers are major health problems, being the most common cancers worldwide. Resistance to apoptosis is closely linked to carcinogenesis and enables malignant cells to evade therapy-induced cell death. In the recent past, the increasing understanding of molecular pathways of apoptosis has provided novel targets in cancer therapy. Several drugs, either inhibiting antiapoptotic signalling or actively inducing apoptosis in cancer cells, have already entered clinical trials. Until now, agents targeting apoptosis pathways are primarily being tested alone or in combination with chemotherapy. In the near future, personalized combination therapies will probably be beneficial fo…

Programmed cell deathChemotherapybusiness.industrymedicine.medical_treatmentGastroenterologyCancerApoptosismedicine.disease_causemedicine.diseaseClinical trialGene Expression Regulation NeoplasticTNF-Related Apoptosis-Inducing LigandApoptosisCancer cellImmunologyCancer researchMedicineHumansGastrointestinal cancerbusinessCarcinogenesisGastrointestinal NeoplasmsSignal TransductionGut
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The Inhibitor of Apoptosis (IAPs) in Adaptive Response to Cellular Stress.

2012

Cells are constantly exposed to endogenous and exogenous cellular injuries. They cope with stressful stimuli by adapting their metabolism and activating various “guardian molecules.” These pro-survival factors protect essential cell constituents, prevent cell death, and possibly repair cellular damages. The Inhibitor of Apoptosis (IAPs) proteins display both anti-apoptotic and pro-survival properties and their expression can be induced by a variety of cellular stress such as hypoxia, endoplasmic reticular stress and DNA damage. Thus, IAPs can confer tolerance to cellular stress. This review presents the anti-apoptotic and survival functions of IAPs and their role in the adaptive response to…

Programmed cell deathDNA damageCellCellular homeostasisReviewUPRInhibitor of apoptosisDNA damage responseNF-κBneurodegenerative diseaseMedicinecancerNF-kBlcsh:QH301-705.5Caspasebiologybusiness.industryEndoplasmic reticulumapoptosisGeneral MedicineCell biologyIAPsmedicine.anatomical_structurelcsh:Biology (General)caspasesApoptosisImmunologyTNFRbiology.proteinbusinessCells
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Deglycosylated bleomycin induces apoptosis in lymphoma cell via c-jun NH2-terminal kinase but not reactive oxygen species

2007

Bleomycin (BLM) has demonstrated potent activity in treating malignant lymphomas but its therapeutic efficacy is hampered by induction of lung fibrosis. This side effect is related to the ability of the drug to generate reactive oxygen species in lung cells. In the present study, we evaluated the consequences of deglycosylation of BLM in term of cytotoxic activity and generation of reactive oxygen species. When tested on U937 human lymphoma cells, both compounds generated a typical apoptotic phenotype. Cell death induction was associated with Bax oligomerization, dissipation of the mitochondrial membrane potential, release of cytochrome c, caspase activation, chromatin condensation and inte…

Programmed cell deathFas Ligand ProteinLymphomaCellApoptosisDNA FragmentationBiologymedicine.disease_causeBiochemistryTNF-Related Apoptosis-Inducing LigandBleomycinmedicineHumansDeath domainPharmacologychemistry.chemical_classificationReactive oxygen speciesAntibiotics AntineoplasticU937 cellCytochrome cJNK Mitogen-Activated Protein KinasesU937 CellsMolecular biologymedicine.anatomical_structurechemistryBiochemistryApoptosisCaspasesbiology.proteinReactive Oxygen SpeciesOxidative stressBiochemical Pharmacology
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