Search results for "Cell Death"

showing 10 items of 824 documents

Glutathione in metastases: From mechanisms to clinical applications.

2016

Metastatic spread, not primary tumors, is the leading cause of cancer death. Glutathione (γ-glutamyl-cysteinyl-glycine, GSH) is particularly relevant in cancer cells as it is involved in regulating carcinogenic mechanisms, growth and dissemination, and multidrug and radiation resistance. Upon interaction of metastatic cells with the vascular endothelium, a high percentage of metastatic cells with high GSH levels survive the combined nitrosative and oxidative stresses elicited by the vascular endothelium. GSH release from different organs, mainly the liver, and its interorgan transport through the blood circulation to metastatic foci, promote their growth. This review focuses on the relation…

0301 basic medicineProgrammed cell deathClinical BiochemistryCancer therapyOxidative phosphorylationBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineMetastatic cellNeoplasmsmedicineAnimalsHumansNeoplasm MetastasisCarcinogenBiochemistry (medical)CancerGlutathionemedicine.diseaseGlutathione030104 developmental biologychemistry030220 oncology & carcinogenesisCancer cellImmunologyCancer researchCritical reviews in clinical laboratory sciences
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Betulinic Acid Kills Colon Cancer Stem Cells

2016

Cancer stem cells (CSCs) are considered to be the origin of cancer and it is suggested that they are resistant to chemotherapy. Current therapies fail to eradicate CSCs and therefore selecting a resistant cell subset that is able to facilitate tumor recurrences. Betulinic acid (BetA) is a broad acting natural compound, shown to induce cell death via the inhibition of the stearoyl-CoA- desaturase (SCD- 1). This enzyme converts saturated fatty acids into unsaturated fatty acids and is over-expressed in tumor cells. Here we show that BetA induces rapid cell death in all colon CSCs tested and is able to affect the CSCs directly as shown, via the loss of clonogenic capacity. Similar results were…

0301 basic medicineProgrammed cell deathColorectal cancerMedicine (miscellaneous)Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCancer stem cellBetulinic acidCell Line TumormedicineHumansEnzyme InhibitorsClonogenic assayCell DeathCancer stem cellStearoyl CoA-desaturaseCancerGeneral Medicinemedicine.diseaseBetulinic acidTriterpenesClone CellsColon cancerTumor resistance030104 developmental biologychemistryBiochemistryCell culture030220 oncology & carcinogenesisCancer treatmentColonic NeoplasmsMutationCancer researchNeoplastic Stem CellsStem cellSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioPentacyclic TriterpenesStearoyl-CoA DesaturaseCurrent stem cell research & therapy
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BAX inhibitor-1 is a Ca(2+) channel critically important for immune cell function and survival.

2015

The endoplasmic reticulum (ER) serves as the major intracellular Ca(2+) store and has a role in the synthesis and folding of proteins. BAX (BCL2-associated X protein) inhibitor-1 (BI-1) is a Ca(2+) leak channel also implicated in the response against protein misfolding, thereby connecting the Ca(2+) store and protein-folding functions of the ER. We found that BI-1-deficient mice suffer from leukopenia and erythrocytosis, have an increased number of splenic marginal zone B cells and higher abundance and nuclear translocation of NF-κB (nuclear factor-κ light-chain enhancer of activated B cells) proteins, correlating with increased cytosolic and ER Ca(2+) levels. When put into culture, purifie…

0301 basic medicineProgrammed cell deathCytoplasmEncephalomyelitis Autoimmune ExperimentalCell SurvivalT-LymphocytesActive Transport Cell NucleusApoptosisBiologyEndoplasmic Reticulum03 medical and health sciencesAnimalsCalcium SignalingObesityMolecular BiologyCalcium signalingMice KnockoutOriginal PaperB-LymphocytesBAX inhibitor 1Endoplasmic reticulumNF-kappa BMembrane ProteinsCell BiologyLeukopeniaNFKB1Acquired immune systemCell biologyEnzyme ActivationMice Inbred C57BLCytosol030104 developmental biologyApoptosisCaspasesCalciumFemaleSpleen
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A naturally occuring triterpene saponin ardisiacrispin B displayed cytotoxic effects in multi-factorial drug resistant cancer cells via ferroptotic a…

2018

WOS: 000432722700010

0301 basic medicineProgrammed cell deathCytotoxicitySaponinPharmaceutical ScienceApoptosisFlow cytometryCell Cycle Distribution03 medical and health sciencesArdisiacrispin BCell Line TumorDrug DiscoverymedicineFerroptosisHumansCytotoxic T cellOleanolic AcidCytotoxicityCaspaseMembrane Potential MitochondrialPharmacologybiologymedicine.diagnostic_testMitochondrial Membrane PotentialChemistryHep G2 CellsSaponinsHCT116 Cellsmedicine.diseaseAntineoplastic Agents PhytogenicDrug Resistance MultipleLeukemia030104 developmental biologyComplementary and alternative medicineDoxorubicinDrug Resistance NeoplasmApoptosisCaspasesCancer cellbiology.proteinCancer researchMolecular MedicineReactive Oxygen SpeciesPhytomedicine
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Docosahexaenoic Acid Attenuates Mitochondrial Alterations and Oxidative Stress Leading to Cell Death Induced by Very Long-Chain Fatty Acids in a Mous…

2020

In the case of neurodegenerative pathologies, the therapeutic arsenal available is often directed towards the consequences of the disease. The purpose of this study is, therefore, to evaluate the ability of docosahexaenoic acid (DHA), a molecule present in certain foods and considered to have health benefits, to inhibit the cytotoxic effects of very long-chain fatty acids (C24:0, C26:0), which can contribute to the development of some neurodegenerative diseases. The effect of DHA (50 &micro

0301 basic medicineProgrammed cell deathDocosahexaenoic AcidsCell SurvivalVery long chain fatty acidoligodendrocytesvery long-chain fatty acidmedicine.disease_causeCatalysisArticleCell Linelcsh:ChemistryInorganic Chemistry03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinemedicineAnimalsViability assayPropidium iodidePhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyMembrane Potential MitochondrialOrganic ChemistryAutophagyFatty Acidsfood and beveragesGeneral Medicinelipotoxicitydocosahexaenoic acidComputer Science ApplicationsCell biologyMitochondriaOligodendrogliaOxidative Stress030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryLipotoxicityDocosahexaenoic acidModels Animallipids (amino acids peptides and proteins)Reactive Oxygen Species030217 neurology & neurosurgeryOxidative stressInternational Journal of Molecular Sciences
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Triclosan-Evoked Neurotoxicity Involves NMDAR Subunits with the Specific Role of GluN2A in Caspase-3-Dependent Apoptosis

2018

Triclosan (TCS) is an antimicrobial agent that is used extensively in personal care and in sanitising products. A number of studies have shown the presence of TCS in different human tissues such as blood, adipose tissue, the liver, brain as well as in breast milk and urine. N-Methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion channels that are widely expressed in the central nervous system and which play key roles in excitatory synaptic transmission. There is, however, no data on the involvement of NMDAR subunits in the apoptotic and neurotoxic effects of TCS. Our experiments are the first to show that TCS used at environmentally relevant concentrations evoked NMDA-dependent effe…

0301 basic medicineProgrammed cell deathGluN1Protein subunitNeurotoxinsNeuroscience (miscellaneous)Glutamic AcidCaspase 3ApoptosisReceptors N-Methyl-D-AspartateArticle03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicinemedicineAnimalsGene SilencingRNA MessengerReceptorNeuronsL-Lactate DehydrogenaseChemistryCaspase 3fungiNeurotoxicityROSTransfectionmedicine.diseaseTriclosanCell biologyGluN2BGluN2AProtein Subunits030104 developmental biologyNeurologyNMDAApoptosisNMDA receptorFemale030217 neurology & neurosurgeryMolecular Neurobiology
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Metabolic Imaging in Multicellular Spheroids of Oncogene-transfected Fibroblasts

2000

Four rat embryo fibroblast (REF) cell lines with defined oncogenic transformation were used to study the relationship between tumorigenic conversion, metabolism, and development of cell death in a 3D spheroid system. Rat1 (spontaneously immortalized) and M1 ( myc-transfected) fibroblasts represent early nontumorigenic transformation stages, whereas Rat1-T1 (T24Ha- ras-transfected Rat1) and MR1 ( myc/T24Ha- ras-co-transfected REF) cells express a highly tumorigenic phenotype. Localized ATP, glucose, and lactate concentrations in spheroid median sections were determined by imaging bioluminescence. ATP concentrations were low in the nonproliferating Rat1 aggregates despite sufficient oxygen an…

0301 basic medicineProgrammed cell deathHistologyGenes mycApoptosisBiology030218 nuclear medicine & medical imaging03 medical and health sciencesAdenosine Triphosphate0302 clinical medicineSpheroids CellularImage Processing Computer-AssistedmedicineAnimalsFrozen SectionsLactic AcidFibroblastCell Line Transformed030102 biochemistry & molecular biologyOncogeneSpheroidEmbryoTransfectionMetabolismMolecular biologyRats Inbred F344RatsCell biologyGenes rasGlucosemedicine.anatomical_structureCell cultureLuminescent Measurementsembryonic structuresAnatomyCell DivisionJournal of Histochemistry & Cytochemistry
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Peroxisome proliferator-activated receptor-γ coactivator-1α mediates neuroprotection against excitotoxic brain injury in transgenic mice: role of mit…

2016

Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is a transcriptional coactivator involved in the regulation of mitochondrial biogenesis and cell defense. The functions of PGC-1α in physiology of brain mitochondria are, however, not fully understood. To address this we have studied wild-type and transgenic mice with a two-fold overexpression of PGC-1α in brain neurons. Data showed that the relative number and basal respiration of brain mitochondria were increased in PGC-1α transgenic mice compared with wild-type mitochondria. These changes occurred concomitantly with altered levels of proteins involved in oxidative phosphorylation (OXPHOS) as studied by proteomi…

0301 basic medicineProgrammed cell deathKainic acidTransgenebcl-X ProteinPeroxisome proliferator-activated receptorBiologyInhibitor of apoptosisSettore BIO/09 - FisiologiaNeuroprotectionOxidative PhosphorylationInhibitor of Apoptosis ProteinsMice03 medical and health scienceschemistry.chemical_compoundXIAP0302 clinical medicineBrain InjurieInhibitor of Apoptosis ProteinAnimalsCA1 Region HippocampalCells CulturedNeuronschemistry.chemical_classificationNeuroscience (all)Kainic AcidCell DeathAnimalNeuron survivalGeneral NeuroscienceProteomicXIAP; Kainic acid; Mitochondria; Neuron survival; PGC-1α; Proteomics; Animals; Brain Injuries; CA1 Region Hippocampal; Cell Death; Cells Cultured; Inhibitor of Apoptosis Proteins; Kainic Acid; Mice; Mitochondria; Neurons; Oxidative Phosphorylation; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Proto-Oncogene Proteins c-bcl-2; bcl-X Protein; Neuroscience (all)NeuronPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaCell biologyXIAP030104 developmental biologyProto-Oncogene Proteins c-bcl-2chemistryMitochondrial biogenesisBrain InjuriesImmunologyPGC-1α030217 neurology & neurosurgeryEuropean Journal of Neuroscience
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Biological activity of PtIV prodrugs triggered by riboflavin-mediated bioorthogonal photocatalysis

2018

AbstractWe have recently demonstrated that riboflavin (Rf) functions as unconventional bioorthogonal photocatalyst for the activation of PtIV prodrugs. In this study, we show how the combination of light and Rf with two PtIV prodrugs is a feasible strategy for light-mediated pancreatic cancer cell death induction. In Capan-1 cells, which have high tolerance against photodynamic therapy, Rf-mediated activation of the cisplatin and carboplatin prodrugs cis,cis,trans-[Pt(NH3)2(Cl)2(O2CCH2CH2CO2H)2] (1) and cis,cis,trans-[Pt(NH3)2(CBDCA)(O2CCH2CH2CO2H)2] (2, where CBDCA = cyclobutane dicarboxylate) resulted in pronounced reduction of the cell viability, including under hypoxia conditions. Such …

0301 basic medicineProgrammed cell deathLightOrganoplatinum CompoundsDNA damageCell SurvivalRiboflavinlcsh:MedicinePlatinum prodrugs DNA bioorthogonal photocatalysis riboflavinAntineoplastic AgentsArticle03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumormedicineHumansProdrugsViability assaylcsh:ScienceCisplatinMultidisciplinaryChemistrylcsh:RProdrugPhotochemical ProcessesChemical biologyCarboplatinCoordination chemistry030104 developmental biologySettore CHIM/03 - Chimica Generale E InorganicaCell culture030220 oncology & carcinogenesisBiophysicslcsh:QBioorthogonal chemistrymedicine.drug
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Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.

2017

The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF…

0301 basic medicineProgrammed cell deathLiver tumorCell SurvivalNecroptosisMice TransgenicBiologyChronic liver diseaseProinflammatory cytokine03 medical and health sciencesLiver diseaseMiceLiver Neoplasms ExperimentalmedicineAnimalsDiethylnitrosamineKinase activityTranscription Factor RelAGeneral Medicinemedicine.disease3. Good healthNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticReceptors Tumor Necrosis Factor Type IHepatocyteReceptor-Interacting Protein Serine-Threonine KinasesCancer researchHepatocytesSignal TransductionResearch ArticleThe Journal of clinical investigation
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