Search results for "G2 Phase"

showing 10 items of 34 documents

Beauvericin-induced cytotoxicity via ROS production and mitochondrial damage in Caco-2 cells.

2013

The cytotoxicity of beauvericin (BEA) on human colon adenocarcinoma (Caco-2) cells was studied as a function of time. Moreover, the oxidative damage and cell death endpoints were monitored after 24, 48 and 72 h. After BEA exposure, the IC₅₀ values ranged from 1.9 ± 0.7 to 20.6 ± 6.9 μM. A decrease in reduced glutathione (GSH; 31%) levels, as well as an increase in oxidized glutathione (GSSG, 20%) was observed. In the presence of BEA, reactive oxygen species (ROS) level was highly increased at an early stage with the highest production of 2.0-fold higher than the control that was observed at 120 min. BEA induced cell death by mitochondria-dependent apoptotic process with loss of the mitochon…

G2 PhaseProgrammed cell deathDNA damageCell SurvivalApoptosisBiologyToxicologymedicine.disease_causechemistry.chemical_compoundInhibitory Concentration 50NecrosisDepsipeptidesmedicineHumansIntestinal Mucosachemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesIonophoresCell growthGeneral MedicineGlutathioneMycotoxinsMolecular biologyGlutathioneBeauvericinCell biologyMitochondriaKineticsOxidative StresschemistryApoptosisLipid PeroxidationCaco-2 CellsReactive Oxygen SpeciesOxidation-ReductionOxidative stressDNA DamageToxicology letters
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TTAS a New Stilbene Derivative that Induces Apoptosis in Leishmania Infantum

2012

Leishmania parasites are able to undergo apoptosis (programmed cell death), similarly to mammalian cells. Recently it was demonstrated in vitro the anti-leishmanial effect of some natural and synthetic stilbenoids including resveratrol and piceatannol. In this study we evaluated the Leishmanicidal activity of a pool of stilbene derivatives which had previously shown high apoptotic efficacy against neoplastic cells. All the compounds tested were capable to decrease the parasite viability in a dose-dependent manner. Trans-stilbenes proved to be markedly more effective than cis-isomers. This was different from that observed in tumor cells in which cis-stilbenes were more potent cytotoxic agent…

G2 PhaseProgrammed cell deathLeishmaniasiSettore MED/17 - Malattie InfettiveImmunologyAntiprotozoal AgentsTUBULINApoptosisResveratrolChromatography AffinityLethal Dose 50chemistry.chemical_compoundGranulocyte-Macrophage Progenitor CellsAnnexin A5Leishmania infantumCytotoxicityCells CulturedMembrane Potential MitochondrialPiceatannolDose-Response Relationship DrugbiologyGeneral MedicineFlow CytometryHematopoietic Stem Cellsbiology.organism_classificationLeishmaniaPROGRAMMED CELL DEATHIn vitroInfectious DiseaseschemistryBiochemistrySTILBENESAntimony Sodium GluconateApoptosisStilbeneElectrophoresis Polyacrylamide GelParasitologyLeishmania infantumCell DivisionLEISHMANIASIS
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Staurosporine-induced apoptosis in Chang liver cells is associated with down-regulation of Bcl-2 and Bcl-XL.

2004

A potent inhibitor of serine/threonine kinases, staurosporine exerts antiproliferative and apoptotic effects in many cancer cells, although the exact mechanism of its action is still unclear. This study examines the effects of staurosporine on Chang liver cells, an immortalized non-tumor cell line, in comparison with those caused in HuH-6 and HepG2 cells, two human hepatoma cell lines. Our results provide evidence that staurosporine promotes apoptosis in Chang liver cells as observed by flow cytometric analysis and acridine orange/ethidium bromide staining. The effect appeared already after 8 h of treatment and increased with treatment time and dose. After 48 h of exposure to 200 nM stauros…

G2 PhaseProgrammed cell deathTime FactorsCell SurvivalLiver cytologyBlotting Westernbcl-X ProteinDown-RegulationMitosisApoptosisBcl-xLAmino Acid Chloromethyl KetonesCell LineMembrane PotentialsEthidiumSettore BIO/10 - BiochimicaGeneticsmedicineHumansStaurosporineEnzyme InhibitorsBcl-2 family factors.CaspaseApoptosis staurosporineDose-Response Relationship DrugbiologyCaspase 3Cell CycleGeneral MedicineFlow CytometryStaurosporineMolecular biologyAcridine OrangeMitochondriaEnzyme ActivationLiverProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCaspasesCancer cellbiology.proteinCell Divisionmedicine.drug
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Curcumin and trans-resveratrol exert cell cycle-dependent radioprotective or radiosensitizing effects as elucidated by the PCC and G2-assay

2013

Curcumin and trans-resveratrol are well-known antioxidant polyphenols with radiomodulatory properties, radioprotecting non-cancerous cells while radiosensitizing tumor cells. This dual action may be the result of their radical scavenging properties and their effects on cell-cycle checkpoints that are activated in response to radiation-induced chromosomal damage. It could be also caused by their effect on regulatory pathways with impact on detoxification enzymes, the up-regulation of endogenous protective systems, and cell-cycle-dependent processes of DNA damage. This work aims to elucidate the mechanisms underlying the dual action of these polyphenols and investigates under which conditions…

G2 PhaseRadiation-Sensitizing AgentsRadiosensitizerCurcuminAntioxidantDNA damageHealth Toxicology and Mutagenesismedicine.medical_treatmentRadioprotectorCellRadiation-Protective AgentsCHO CellsBiologyRadiation ToleranceCell Fusionchemistry.chemical_compoundCricetulusCricetinaeStilbenesGeneticsmedicineAnimalsHumansRadiosensitivityMolecular BiologyCells CulturedMutagenicity TestsCell CycleCell cycleChromatin Assembly and DisassemblyRadiosensitizermedicine.anatomical_structureG2-assayBiochemistrychemistryResveratrolPeripheral blood lymphocyteCancer researchCurcumintrans-ResveratrolPremature chromosome condensationMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Type III Secretion-Dependent Cell Cycle Block Caused in HeLa Cells by Enteropathogenic Escherichia coliO103

2001

ABSTRACT Rabbit enteropathogenic Escherichia coli (EPEC) O103 induces in HeLa cells an irreversible cytopathic effect characterized by the recruitment of focal adhesions, formation of stress fibers, and inhibition of cell proliferation. We have characterized the modalities of the proliferation arrest and investigated its underlying mechanisms. We found that HeLa cells that were exposed to the rabbit EPEC O103 strain E22 progressively accumulated at 4C DNA content and did not enter mitosis. A significant proportion of the cells were able to reinitiate DNA synthesis without division, leading to 8C DNA content. This cell cycle inhibition by E22 was abrogated in mutants lacking EspA, -B, and -D…

G2 Phase[SDV]Life Sciences [q-bio]ImmunologyCyclin BMitosisReceptors Cell SurfacePATHOGENICITECyclin BMicrobiology03 medical and health sciencesBacterial ProteinsCDC2 Protein KinaseEscherichia coliHumansCyclin B1PhosphorylationCyclin B1Adhesins BacterialMitosisCytoskeleton030304 developmental biologyIntimin0303 health sciencesCyclin-dependent kinase 1Cellular Microbiology: Pathogen-Host Cell Molecular Interactionsbiology030306 microbiologyCell growthEscherichia coli ProteinsCell CycleREARRANGEMENTCell cycle[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyCell biology[SDV] Life Sciences [q-bio]Infectious Diseasesbiology.proteinTyrosineParasitologyCarrier ProteinsCDC2 Protein KinaseBacterial Outer Membrane ProteinsHeLa Cells
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Synthesis and antiproliferative activity of thiazolyl-bis-pyrrolo[2,3-b]pyridines and indolyl-thiazolyl-pyrrolo[2,3-c]pyridines, nortopsentin analogu…

2015

Two new series of nortopsentin analogues, in which the imidazole ring of the natural product was replaced by thiazole and indole units were both substituted by 7-azaindole moieties or one indole unit was replaced by a 6-azaindole portion, were efficiently synthesized. Compounds belonging to both series inhibited the growth of HCT-116 colorectal cancer cells at low micromolar concentrations, whereas they did not affect the viability of normal-like intestinal cells. A compound of the former series induced apoptosis, evident as externalization of plasma membrane phosphatidylserine (PS), and changes of mitochondrial trans-membrane potential, while blocking the cell cycle in G2/M phase. In contr…

G2 Phaseantiproliferative activitybis-indolyl alkaloidsStereochemistryPyridinesPharmaceutical ScienceNortopsentin analoguesthiazolyl-bis-pyrrolo [23-b]pyridinesVacuoleArticlechemistry.chemical_compoundDrug DiscoveryImidazoleHumansPyrrolesautophagic deathThiazolelcsh:QH301-705.5Pharmacology Toxicology and Pharmaceutics (miscellaneous)Cell ProliferationIndole testMembrane Potential MitochondrialnortopsentinsDose-Response Relationship DrugMolecular Structureindolyl-thiazolyl-pyrrolo[23-c]pyridinesthiazolyl-bis-pyrrolo[23-b]pyridinesapoptosisPhosphatidylserineCell cycleHCT116 CellsSettore CHIM/08 - Chimica Farmaceuticaindolyl-thiazolyl-pyrrolo[23-<i>c</i>]pyridinesThiazoleslcsh:Biology (General)chemistryCytoplasmApoptosismarine alkaloidsthiazolyl-bis-pyrrolo [23-<i>b</i>]pyridinesMarine drugs
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3-[4-(1H-indol-3-yl)-1,3-thiazol-2-yl]-1H-pyrrolo[2,3-b]pyridines, nortopsentin Analogues with antiproliferative activity

2015

A new series of nortopsentin analogues, in which the imidazole ring of the natural product was replaced by thiazole and the indole unit bound to position 2 of the thiazole ring was substituted by a 7-azaindole moiety, was efficiently synthesized. Two of the new nortopsentin analogues showed good antiproliferative effect against the totality of the NCI full panel of human tumor cell lines (~60) having GI50 values ranging from low micromolar to nanomolar level. The mechanism of the antiproliferative effect of these derivatives, investigated on human hepatoma HepG2 cells, was pro-apoptotic, being associated with externalization of plasma membrane phosphatidylserine and mitochondrial dysfunctio…

IndolesHalogenationPyridines3-b]pyridinesPharmaceutical ScienceApoptosisAntiproliferative activity3-[4-(1<i>H</i>-indol-3-yl)-13-thiazol-2-yl]-1<i>H</i>-pyrrolo[23-<i>b</i>]pyridineschemistry.chemical_compoundNeoplasmsDrug DiscoveryImidazoleMoietyindolyl alkaloidsPharmacology Toxicology and Pharmaceutics (miscellaneous)lcsh:QH301-705.5Membrane Potential MitochondrialMolecular Structure3-[4-(1H-indol-3-yl)-1; 3-thiazol-2-yl]-1H-pyrrolo[2; 3-b]pyridines; Antiproliferative activity; Indolyl alkaloids; Marine alkaloids; Nortopsentin analogues; Drug Discovery3003 Pharmaceutical ScienceImidazolesPhosphatidylserineMitochondrianortopsentin analoguesIndolyl alkaloidmarine alkaloidsG2 PhaseStereochemistryNortopsentin analogueAntineoplastic AgentsMethylationResting Phase Cell CycleArticleAlkaloids3-[4-(1H-indol-3-yl)-1Cell Line TumorHumansPyrroles3-[4-(1H-indol-3-yl)-13-thiazol-2-yl]-1H-pyrrolo[23-b]pyridines3-thiazol-2-yl]-1H-pyrrolo[2ThiazoleCell ProliferationIndole testNatural productCell growthDrug Discovery3003 Pharmaceutical ScienceSettore CHIM/08 - Chimica FarmaceuticaThiazoleschemistrylcsh:Biology (General)Cell cultureDrug DesignMarine alkaloid3-[4-(1H-indol-3-yl)-13-thiazol-2-yl]-1H-pyrrolo[23-b]pyridine
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Study of the cytolethal distending toxin (CDT)-activated cell cycle checkpoint. Involvement of the CHK2 kinase.

2001

AbstractThe bacterial cytolethal distending toxin (CDT) triggers a G2/M cell cycle arrest in eukaryotic cells by inhibiting the CDC25C phosphatase-dependent CDK1 dephosphorylation and activation. We report that upon CDT treatment CDC25C is fully sequestered in the cytoplasmic compartment, an effect that is reminiscent of DNA damage-dependent checkpoint activation. We show that the checkpoint kinase CHK2, an upstream regulator of CDC25C, is phosphorylated and activated after CDT treatment. In contrast to what is observed with other DNA damaging agents, we demonstrate that the activation of CHK2 can only take place during S-phase. Use of wortmannin and caffeine suggests that this effect is no…

Intracellular FluidCell cycle checkpointCytolethal distending toxinCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiochemistryS PhaseWortmanninchemistry.chemical_compoundStructural BiologyPhosphorylation0303 health sciences030302 biochemistry & molecular biologyCell CycleCell cycleProtein-Tyrosine Kinases3. Good healthCell biologyDNA-Binding Proteinsbiological phenomena cell phenomena and immunityWortmanninG2 PhaseCytolethal distending toxinBacterial ToxinsProto-Oncogene Proteins pp60(c-src)Biophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesCell Line03 medical and health sciencesCaffeineGeneticsHumanscdc25 PhosphatasesCHEK1Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biologyCheckpoint 2 kinaseCyclin-dependent kinase 1Cell growthTumor Suppressor ProteinsCell BiologyG2-M DNA damage checkpointCDC25CAndrostadienesGenes cdcchemistryCancer researchHeLa CellsFEBS letters
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Fibroblasts from bank voles inhabiting Chernobyl have increased resistance against oxidative and DNA stresses

2018

Background Elevated levels of environmental ionizing radiation can be a selective pressure for wildlife by producing reactive oxygen species and DNA damage. However, the underlying molecular mechanisms that are affected are not known. Results We isolated skin fibroblasts from bank voles (Myodes glareolus) inhabiting the Chernobyl nuclear power plant accident site where background radiation levels are about 100 times greater than in uncontaminated areas. After a 10 Gy dose of gamma radiation fibroblasts from Chernobyl animals recovered faster than fibroblasts isolated from bank voles living in uncontaminated control area. The Chernobyl fibroblasts were able to sustain significantly higher do…

Male0301 basic medicinep53Antioxidantmedicine.medical_treatment010501 environmental sciences01 natural sciencesAntioxidantsIonizing radiationsäteilybiologiachemistry.chemical_classificationCell DeathbiologyArvicolinaelcsh:CytologyBank volefibroblastitOxidantshumanitiesCell biologyAntioxidant capacityBank voleResearch ArticleG2 PhaseCell SurvivalDNA damagemetsämyyräOxidative phosphorylationCell LineMicrobiologyChernobyl03 medical and health sciencesmedicineAnimalsEnvironmental ionizing radiationlcsh:QH573-671Geneoksidatiivinen stressi0105 earth and related environmental sciencesantioksidantitReactive oxygen speciesCell Cycle CheckpointsDNACell BiologyFibroblastsbiology.organism_classificationresistenssiOxidative Stress030104 developmental biologyChernobyl Nuclear AccidentchemistryGamma RaysApoptosisbank volesDNA damageTumor Suppressor Protein p53BMC Cell Biology
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DNA strand breaks induced by nuclear hijacking of neuronal NOS as an anti-cancer effect of 2-methoxyestradiol

2015

2-Methoxyestradiol (2-ME) is a physiological metabolite of 17β-estradiol. At pharmacological concentrations, 2-ME inhibits colon, breast and lung cancer in tumor models. Here we investigated the effect of physiologically relevant concentrations of 2-ME in osteosarcoma cell model. We demonstrated that 2-ME increased nuclear localization of neuronal nitric oxide synthase, resulting in nitro-oxidative DNA damage. This in turn caused cell cycle arrest and apoptosis in osteosarcoma cells. We suggest that 2-ME is a naturally occurring hormone with potential anti-cancer properties.

Pathologymedicine.medical_specialtyneuronal nitric oxide synthaseCell cycle checkpoint2-methoxyestradiolDNA damageAntineoplastic AgentsApoptosisBone NeoplasmsNitric Oxide Synthase Type Imedicine.disease_causeNitric OxideNitric oxidechemistry.chemical_compoundReactive nitrogen specieCell Line TumormedicineHumans2-MethoxyestradiolReactive nitrogen speciesCytokinesisOsteosarcomaEstradiolbusiness.industryDNA BreaksIntracellular Signaling Peptides and ProteinsCancermedicine.diseaseReactive Nitrogen SpeciesG2 Phase Cell Cycle CheckpointsOxidative StressOncologychemistryApoptosis2-methoxyestradiol; Neuronal nitric oxide synthase; Nitric oxide; Osteosarcoma; Reactive nitrogen species; OncologyCancer researchM Phase Cell Cycle CheckpointsbusinessTumor Suppressor p53-Binding Protein 1Oxidative stressmedicine.drugResearch Paper
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