Search results for "Cytometry"

showing 10 items of 852 documents

The Synthetic Cannabinoid WIN 55,212-2 Sensitizes Hepatocellular Carcinoma Cells to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-I…

2010

In this article, we demonstrate that the synthetic cannabinoid R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)-(1-naphthalenyl) methanone mesylate (WIN 55,212-2) sensitizes human hepatocellular carcinoma (HCC) cells to apoptosis mediated by tumor necrosis-related apoptosis inducing ligand (TRAIL). The apoptotic mechanism induced by treatment with WIN/TRAIL combination involved the loss of the mitochondrial transmembrane potential and led to the activation of caspases. In HCC cells, WIN treatment induced the up-regulation of TRAIL death receptor DR5, an effect that seemed to be related to the increase in the level of p8 and CHOP, two factors implicat…

Carcinoma HepatocellularDNA ComplementaryMorpholinesApoptosisNaphthalenesCHOPMembrane PotentialsTNF-Related Apoptosis-Inducing LigandCell Line TumorSurvivinmedicineHumansWIN 55212-2Protein kinase BTranscription factorCaspaseDNA PrimersPharmacologybiologyCannabinoidsReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsGene AmplificationDNA NeoplasmFlow CytometryBenzoxazinesReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMitochondrial MembranesImmunologybiology.proteinCancer researchMolecular MedicineTumor necrosis factor alphaTranscription Factor CHOPmedicine.drugMolecular Pharmacology
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Human HepG2 and rat Fao hepatic-derived cell lines show different responses to ciprofibrate, a peroxisome proliferator: analysis by flow cytometry.

1996

Abstract Peroxisome proliferators, and especially hypolipidemic drugs such as ciprofibrate, are known to be hepatocarcinogens in rodents, but their effect in humans is controversial. In an attempt to investigate the effects of ciprofibrate at a cellular level, the analysis of individual whole cells was performed by flow cytometry on samples from two hepatic-derived cell lines: the rat Fao cell line and the human HepG2 cell line. The increase of light scatter signals in rat Fao cells treated for 3 days with ciprofibrate at 250 μMwas related to modifications of intrinsic cellular parameters, such as size and cytoplasmic granularity. Conversely, no variations appeared in human HepG2-treated ce…

Carcinoma HepatocellularLightPeroxisome ProliferationBiologyCytoplasmic GranulesMicrobodiesFlow cytometryClofibric AcidmedicineTumor Cells CulturedAnimalsHumansScattering RadiationCell SizeHypolipidemic Agentschemistry.chemical_classificationOxidase testmedicine.diagnostic_testCell CycleLiver NeoplasmsFibric AcidsCell BiologyDNA NeoplasmCell cycleFlow CytometryCell biologyRatsEnzymeBiochemistrychemistryLiverCytoplasmCell cultureCiprofibrateOxidoreductasesCell Divisionmedicine.drugExperimental cell research
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Induction of apoptosis and inhibition of cell growth in human hepatocellular carcinoma cells by COX-2 inhibitors

2005

The aim of the present study was to examine the effects of nonselective (indomethacin) and selective cyclooxygenase-2 (COX-2) inhibitors (NS-398, nimesulide, and CAY10404) on cell growth, cell cycle distribution, and apoptosis in three human hepatocellular carcinoma cell lines (HepG2, HuH-6, and HA22T/VGH) with different characteristics of differentiation and biological behavior. The four COX inhibitors showed a dose-dependent growth-inhibitory effect in all the cell lines. No substantial arrests in the progression of the cells through the cell cycle were observed after treatment of HuH-6 or HA22T/VGH for 48 h with the various inhibitors. On the other hand, there were significant increases …

Carcinoma HepatocellularTime FactorsApoptosisPharmacologyBiologyGeneral Biochemistry Genetics and Molecular BiologyFlow cytometryInhibitory Concentration 50History and Philosophy of ScienceCell Line TumorCarcinomamedicineHumansProtein IsoformsCyclooxygenase InhibitorsEnzyme InhibitorsCell ProliferationCyclooxygenase 2 InhibitorsDose-Response Relationship DrugNeovascularization Pathologicmedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionCell growthGeneral NeuroscienceAnti-Inflammatory Agents Non-SteroidalCell CycleMembrane Proteinsantineoplastic activity apoptosis cancer cell cultureCell cycleFlow Cytometrymedicine.diseaseCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesCell cultureApoptosisHepatocellular carcinomaNimesulidemedicine.drug
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Allogeneic effector/memory Th-1 cells impair FoxP3+ regulatory T lymphocytes and synergize with chaperone-rich cell lysate vaccine to treat leukemia

2011

AbstractTherapeutic strategies combining the induction of effective antitumor immunity with the inhibition of the mechanisms of tumor-induced immunosuppression represent a key objective in cancer immunotherapy. Herein we demonstrate that effector/memory CD4+ T helper-1 (Th-1) lymphocytes, in addition to polarizing type-1 antitumor immune responses, impair tumor-induced CD4+CD25+FoxP3+ regulatory T lymphocyte (Treg) immunosuppressive function in vitro and in vivo. Th-1 cells also inhibit the generation of FoxP3+ Tregs from naive CD4+CD25−FoxP3− T cells by an interferon-γ–dependent mechanism. In addition, in an aggressive mouse leukemia model (12B1), Th-1 lymphocytes act synergistically with …

Cell Extractsmedicine.medical_treatmentBlotting WesternImmunologyMice NudeEnzyme-Linked Immunosorbent Assaychemical and pharmacologic phenomenaMice SCIDBiologyCancer VaccinesT-Lymphocytes RegulatoryBiochemistryInterferon-gammaMiceLymphocytes Tumor-InfiltratingImmune systemCancer immunotherapyAntigenTumor Cells CulturedmedicineAnimalsInterferon gammaIL-2 receptorImmunobiologyMice Inbred BALB CLeukemia ExperimentalFOXP3hemic and immune systemsForkhead Transcription FactorsDendritic CellsT-Lymphocytes Helper-InducerCell BiologyHematologyT lymphocyteFlow Cytometrymedicine.diseaseMice Inbred C57BLLeukemiaImmunologyImmunologic MemoryMolecular ChaperonesT-Lymphocytes Cytotoxicmedicine.drugBlood
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Assessment of Escherichia coli B with enhanced permeability to fluorochromes for flow cytometric assays of bacterial cell function.

2002

Background Flow cytometry has become a choice methodology for microbiological research. However, functional cytometric assays in live bacteria are still limited. This is due, in part, to the cell wall impairing penetration of vital dyes in bacteria, thus imposing permeabilization procedures. These manipulations may affect cell physiology, provoke cell aggregation or lysis, and they are time-consuming. Escherichia coli B strains have been used for mutagenic assays because of an altered lipopolysaccharide that provokes increased membrane permeability. We assessed the use of these strains as possible alternatives for flow cytometric assays to avoid the permeabilization steps. Methods Suspensio…

Cell Membrane PermeabilityMembrane permeabilityBiophysicsBiologymedicine.disease_causePathology and Forensic MedicineFlow cytometrychemistry.chemical_compoundEndocrinologymedicineEscherichia coliPropidium iodideFluorescein isothiocyanateEscherichia coliFluorescent Dyesmedicine.diagnostic_testStaining and LabelingCell BiologyHematologyFlow CytometryMolecular biologyCell aggregationStainingOxidative StresschemistryBiochemistryCytometryCytometry
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Superoxide generation by human neutrophils induced by low doses of Escherichia coli hemolysin.

1991

Escherichia coli hemolysin (Hly) was isolated from bacterial culture supernatants by polyethylene glycol precipitation and centrifugation in glycerol density gradients. The toxin preparations contained less than 1 mol of lipopolysaccharide per 10 mol of protein, and they had no fatty acids. The capacity of purified hemolysin to stimulate superoxide anion production in polymorphonuclear leukocytes was monitored kinetically in a lumimeter by using the lucigenin assay and was correlated with the kinetics of transmembrane pore formation. When applied to leukocytes suspended in protein-free buffer, very low concentrations (0.02 to 0.1 HU/ml) of the toxin strongly stimulated the production of sup…

Cell Membrane PermeabilityNeutrophilsImmunologyBacterial ToxinsBiologymedicine.disease_causeHemolysin ProteinsMicrobiologychemistry.chemical_compoundHemolysin ProteinsBacterial ProteinsSuperoxidesmedicineEscherichia coliHumansCentrifugationLucigeninEscherichia coliSuperoxideToxinEscherichia coli ProteinsHemolysinFlow CytometryRespiratory burstKineticsInfectious DiseaseschemistryBiochemistryTetradecanoylphorbol AcetateParasitologyPropidiumResearch ArticleInfection and immunity
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Inhibitory effects oftrans-resveratrol analogs molecules on the proliferation and the cell cycle progression of human colon tumoral cells

2008

International audience; Resveratrol may function as a cancer chemopreventive agent. However, few data are available on the antitumoral activities of its dimer, epsilon-viniferin, also present in human diet. So, the effects of resveratrol, epsilon-viniferin, of their acetylated forms (resveratrol triacetate, epsilon-viniferin pentaacetate) and of vineatrol (a wine grape extract) were compared on human adenocarcinoma colon cells. Resveratrol and resveratrol triacetate inhibit cell proliferation and arrest cell cycle. epsilon-Viniferin and epsilon-viniferin pentaacetate slightly reduce cell proliferation. Vineatrol inhibits cell proliferation and favors an accumulation in the S phase of the ce…

Cell Membrane Permeabilityendocrine system diseasesvineatrolMESH: Cell CycleMESH: DNA ReplicationMESH: Flow CytometryresveratrolResveratrolMESH : Antineoplastic Agents PhytogenicWine grapechemistry.chemical_compoundMESH: Structure-Activity RelationshipMESH: StilbenesStilbenesMESH : Structure-Activity RelationshipMESH: Cell Membrane Permeabilityskin and connective tissue diseasesfood and beveragesDNA NeoplasmMESH : Cell DivisionCell cycleFlow CytometryMESH : Colonic Neoplasmscolon cancerBiochemistryColonic NeoplasmsMESH: Cell Divisioncell cycleMESH : DNA NeoplasmCell Divisionhormones hormone substitutes and hormone antagonistsMESH : DNA ReplicationBiotechnologyDNA ReplicationMESH: XenobioticsMESH: Cell Line TumorMESH : Flow CytometryMESH: Antineoplastic Agents PhytogenicMESH: DNA NeoplasmMESH : XenobioticsBiologyXenobioticsMESH : StilbenesStructure-Activity RelationshipCell Line TumorMESH : Cell Cycle[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansStructure–activity relationship[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologypolyphenolsS phaseMESH: Colonic NeoplasmsMESH: HumansMESH : Cell Line TumorCell growthorganic chemicalsMESH : HumansAntineoplastic Agents PhytogenicchemistryMESH : Cell Membrane PermeabilityAcetylationCell cultureCancer researchFood ScienceMolecular Nutrition & Food Research
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Involvement of enniatins-induced cytotoxicity in human HepG2 cells.

2012

Enniatins (ENNs) are mycotoxins found in Fusarium fungi and they appear in nature as mixtures of cyclic depsipeptides. The ability to form ionophores in the cell membrane is related to their cytotoxicity. Changes in ion distribution between inner and outer phases of the mitochondria affect to their metabolism, proton gradient, and chemiosmotic coupling, so a mitochondrial toxicity analysis of enniatins is highly recommended because they host the homeostasis required for cellular survival. Two ENNs, ENN A and ENN B on hepatocarcinoma cells (HepG2) at 1.5 and 3 μM and three exposure times (24, 48 and 72 h) were studied. Flow cytometry was used to examine their effects on cell proliferation, t…

Cell SurvivalApoptosisMitochondrionBiologyToxicologyFlow cytometryCell membraneFusariumDepsipeptidesmedicineCytotoxic T cellHumansCytotoxicityCell ProliferationMembrane Potential Mitochondrialmedicine.diagnostic_testCell growthCell CycleGeneral MedicineHep G2 CellsCell cycleMycotoxinsCell biologyMitochondriamedicine.anatomical_structureApoptosisCell DivisionPropidiumToxicology letters
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Induction of apoptosis by arachidonic acid in human retinoblastoma Y79 cells: involvement of oxidative stress

2000

Arachidonic acid administration caused apoptosis in Y79 cells, as shown by typical morphological changes, phosphatidylserine externalization, chromatin condensation, processing and activation of caspase-3 and cleavage of the endogenous caspase substrate poly-(ADP-ribose)-polymerase. Arachidonic acid also caused lamin B cleavage, suggesting caspase-6 activation. Arachidonic acid treatment was accompanied by increased formation of the lipid peroxidation end products malondialdehyde and 4-hydroxy-2-nonenal, lowering in reduced glutathione content and in mitochondrial membrane potential. Inhibiting glutathione synthesis sensitized Y79 cells to apoptosis-inducing stimuli, whilst replenishing red…

Cell SurvivalBlotting WesternApoptosisCell Countmedicine.disease_causeMembrane PotentialsLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundPhospholipase A2medicineTumor Cells Culturedarachidonic acidHumansCYP2C8biologyDose-Response Relationship DrugRetinoblastomaGlutathioneTrypan BlueMalondialdehydeFlow CytometryGlutathioneSensory SystemsCell biologyMitochondriaOphthalmologyOxidative StressBiochemistrychemistryMitochondrial permeability transition poreCaspasesbiology.proteinArachidonic acidColorimetryPoly(ADP-ribose) PolymerasesOxidative stress
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Cytotoxicity of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide in multidrug-resistant cancer cells through activation of PERK/eIF2α/AT…

2021

After decades of research, multidrug resistance (MDR) remains a huge challenge in cancer treatment. In this study, the cytotoxic of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide (MCC1734) has been investigated towards multidrug-resistant cancer cell lines. MCC1734 exerted cytotoxicity on cell lines expressing different mechanisms of drug resistance (P-glycoprotein, BCRP, ABCB5, EGFR, p53 knockout) to a different extent. Interestingly, sensitive CCRF-CEM cells and multidrug-resistant P-gp-overexpressing CEM/ADR5000 cells represented similar sensitivity towards MCC1734, indicating MCC1734 can bypass P-gp-mediated resistance. Microarray-based mRNA expression revealed that MCC17…

Cell SurvivalEukaryotic Initiation Factor-2Antineoplastic AgentsMitochondrionBiochemistryFlow cytometryeIF-2 KinaseCell Line TumorOxazinesmedicineHumansCytotoxic T cellGene Regulatory NetworksCytotoxicityPharmacologyMolecular Structuremedicine.diagnostic_testChemistryCell cycleActivating Transcription Factor 4Gene Expression Regulation NeoplasticXanthenesDrug Resistance NeoplasmCell cultureApoptosisCancer cellCancer researchGene DeletionBiochemical Pharmacology
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