Search results for "TUMOR CELLS"

showing 10 items of 663 documents

Effect of population patchiness and migration rates on the adaptation and divergence of vesicular stomatitis virus quasispecies populations

1999

The effect of migration among different isolated virus quasispecies populations on their adaptation and diversity was analysed through experimental evolution. Anin vitrocell system was employed to simulate migration of vesicular stomatitis virus between isolated homogeneous host cell populations. The results clearly demonstrated a positive correlation between the migration rate and the magnitude of the mean fitness reached by the virus quasispecies populations. The results also showed, although less clearly, that fitness differences among quasispecies decreased with the magnitude of migration. These results are in close agreement with predictions of standard population genetics theory. Thes…

PopulationAdaptation BiologicalViral quasispeciesBiologyVesicular stomatitis Indiana virusVirusCell LineDivergenceViral Envelope ProteinsCricetinaeVirologyTumor Cells CulturedAnimalsHumanseducationGeneticseducation.field_of_studyExperimental evolutionMembrane GlycoproteinsModels GeneticGenetic Variationbiology.organism_classificationVirologyHomogeneousVesicular stomatitis virusDirected Molecular EvolutionAdaptationJournal of General Virology
researchProduct

Functional size of complement and perforin pores compared by confocal laser scanning microscopy and fluorescence microphotolysis

1991

Abstract Confocal laser scanning microscopy and fluorescence microphotolysis (also referred to as fluorescence photobleaching recovery) were employed to study the transport of hydrophilic fluorescent tracers through complement and perforin pores. By optimizing the confocal effect it was possible to determine the exclusion limit of the pores in situ, i.e. without separation of cells and tracer solution. Single-cell flux measurements by fluorescence microphotolysis yielded information on the sample population distribution of flux rates. By these means a direct comparison of complement and perforin pores was made in sheep erythrocyte membranes. In accordance with previous studies employing a v…

Pore Forming Cytotoxic ProteinsIn situCell Membrane PermeabilityConfocalBiophysicsAntigen-Antibody ComplexIn Vitro TechniquesBiologyBiochemistryTumor Cells CulturedmedicineAnimalsHumansMembrane GlycoproteinsSheepPerforinLasersCell MembraneErythrocyte MembraneMembrane ProteinsComplement System ProteinsCell BiologyFluorescencePhotobleachingCell biologyRed blood cellmedicine.anatomical_structureMembranePerforinMicroscopy Electron Scanningbiology.proteinCytolysinBiochimica et Biophysica Acta (BBA) - Biomembranes
researchProduct

Cytoprotective effect of NMDA receptor antagonists on prion protein (PrionSc)-induced toxicity in rat cortical cell cultures

1993

Rat cortical cells were incubated with the Scrapie prion protein, PrionSc. At concentrations of 3 ng/ml of PrionSc and higher, the viability of the cells decreased significantly after a 12-h incubation period. Simultaneously, the degree of DNA fragmentation increased. In control experiments with antibodies against PrionSc, PrionSc lost its deleterious effect on neurons. PrionSc did not affect the viability of astrocytes. Drugs known to block NMDA receptor channels, such as memantine (1-amino-3,5-dimethyl-adamantane) (Mem), its analogue 1-N-methylamino-3,5-dimethyl-adamantane as well as (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) prevented the effect of …

PrPSc ProteinsCell SurvivalPrionsNerve Tissue ProteinsScrapiePharmacologyReceptors N-Methyl-D-AspartateIncubation periodNeuroblastomaTumor Cells CulturedmedicineAnimalsRats WistarCells CulturedCerebral CortexNeuronsPharmacologybiologyMemantineCalcium Channel BlockersIn vitroRatsAstrocytesLiposomesToxicityImmunologybiology.proteinDNA fragmentationNMDA receptorAntibodymedicine.drugEuropean Journal of Pharmacology: Molecular Pharmacology
researchProduct

Chemically modified tetracyclines induce cytotoxic effects against J774 tumour cell line by activating the apoptotic pathway

2003

Here, we have studied the effects of chemically modified tetracyclines (CMTs) on apoptosis both at the level of the cytoplasmic proteolytic caspase cascade, and on Bcl-2 and c-myc mRNA expression in the J774 macrophage cell line. The results indicate that CMTs induce morphological changes consistent with apoptotic events, as clearly demonstrated both by the acridine orange and ethidium bromide staining, and by TUNEL and fragmentation ELISA assays. Furthermore, the analysis of the cell cycle by flow cytometry shows an evident apoptotic sub-G0G1 peak, without important modifications in the cell cycle distribution. CMTs induce programmed cell death (PCD) in a dose-dependent manner and CMT-8 is…

Programmed cell deathCell SurvivalImmunologyApoptosisProto-Oncogene Proteins c-mycMicechemistry.chemical_compoundTumor Cells CulturedAnimalsImmunology and AllergyRNA MessengerFragmentation (cell biology)CaspasePharmacologyTUNEL assayDose-Response Relationship DrugbiologyAcridine orangeTetracyclineCell cycleMolecular biologyGene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2chemistryTetracyclinesApoptosisCaspasesMacrophages Peritonealbiology.proteinFemaleSignal transductionInternational Immunopharmacology
researchProduct

Differentiation-associated apoptosis of neural stem cells is effected by Bcl-2 overexpression: impact on cell lineage determination

2001

Apoptosis is an integral part of neural development. To elucidate the importance of programmed cell death on cell lineage determination we utilized murine PCC7-Mzl cells, a model system for neural differentiation. Treatment of pluripotent PCC7-Mzl stem cells with 0.1 microM all-trans retinoic acid (RA) causes a cease of proliferation and an initiation of differentiation into neurons, glial cells and fibroblasts. Simultaneously, a fraction of the cell culture (ca. 25%) dies within 24 h by apoptosis. We transfected PCC7-Mzl cells with the human bcl-2 cDNA and generated PCC7-Mz-Bcl-2 cell lines expressing two- to tenfold higher levels of Bcl-2 than parental cells. Overexpression of Bcl-2 resul…

Programmed cell deathDNA ComplementaryHistologyCellular differentiationApoptosisTretinoinBiologyCeramidesTransfectionPathology and Forensic MedicineMiceNeurosphereTumor Cells CulturedAnimalsCell LineageElectrophoresis Agar GelNeuronsCaspase 8Stem CellsCell DifferentiationCell BiologyGeneral MedicineFibroblastsMolecular biologyCaspase 9Neural stem cellCell biologyP19 cellProto-Oncogene Proteins c-bcl-2Cell cultureCaspasesStem cellNeurogliaBiomarkersCell DivisionAdult stem cellEuropean Journal of Cell Biology
researchProduct

ROS-Dependent ER Stress and Autophagy Mediate the Anti-Tumor Effects of Tributyltin (IV) Ferulate in Colon Cancer Cells

2020

Organotin compounds represent potential cancer therapeutics due to their pro-apoptotic action. We recently synthesized the novel organotin ferulic acid derivative tributyltin (IV) ferulate (TBT-F) and demonstrated that it displays anti-tumor properties in colon cancer cells related with autophagic cell death. The purpose of the present study was to elucidate the mechanism of TBT-F action in colon cancer cells. We specifically show that TBT-F-dependent autophagy is determined by a rapid generation of reactive oxygen species (ROS) and correlated with endoplasmic reticulum (ER) stress. TBT-F evoked nuclear factor erythroid-2 related factor 2 (Nrf2)-mediated antioxidant response and Nrf2 silenc…

Programmed cell deathNF-E2-Related Factor 2Glucose-regulated proteinApoptosismedicine.disease_causeArticleCatalysisInorganic Chemistrylcsh:ChemistrySettore BIO/10 - BiochimicaAutophagyTumor Cells CulturedmedicineHumansGene silencingoxidative stressPhysical and Theoretical ChemistryEndoplasmic Reticulum Chaperone BiPMolecular Biologylcsh:QH301-705.5tributyltin (IV) derivativeSpectroscopyCell Proliferationoxidative strebiologyChemistryEndoplasmic reticulumOrganic ChemistryAutophagyCancerROSGeneral Medicineendoplasmic reticulum stremedicine.diseaseComputer Science ApplicationsGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999autophagic cell deathColonic NeoplasmsUnfolded protein responseCancer researchbiology.proteinendoplasmic reticulum stressTrialkyltin CompoundsReactive Oxygen SpeciesOxidative stress
researchProduct

Swelling and death of neuronal cells by lactic acid.

1993

Lactacidosis occurring in cerebral ischemia or trauma is a major mechanism of cytotoxic brain edema and brain damage. Respective effects of lactacidosis were currently analyzed in vitro by employment of the murine neuronal cell line, Neuro-2A, in order to obtain a better understanding of specific mechanisms underlying cell swelling and cell death in comparison with glial cells. The cells were suspended in a physiological medium in the presence of lactic acid at increasing concentrations. Levels of acidosis reaching from pH 6.8-5.6 were obtained while other parameters, such as osmolarity and electrolyte concentrations, were maintained in the physiological range. Assessment of cell swelling a…

Programmed cell deathPathologymedicine.medical_specialtyBiologyFlow cytometryAndrologychemistry.chemical_compoundMiceNeuroblastomamedicineTumor Cells CulturedAnimalsViability assayPropidium iodideLactic AcidAcidosisNeuronsOsmotic concentrationmedicine.diagnostic_testCell DeathOsmolar ConcentrationHydrogen-Ion ConcentrationFlow CytometryCulture MediaNeurologychemistryCell cultureLactatesNeurology (clinical)medicine.symptomSwellingNeurogliaJournal of the neurological sciences
researchProduct

The N-glycan processing in HT-29 cells is a function of their state of enterocytic differentiation. Evidence for an atypical traffic associated with …

1991

International audience; When the human colon cancer cells HT-29 undergo enterocytic differentiation, they correctly process their N-glycans, whereas their undifferentiated counterpart are unable to process Man9-8-GlcNAc2 species, the natural substrate of alpha-mannosidase I. As this enzyme is fully active in both HT-29 cell populations, we hypothesize that N-glycoproteins are unable to reach the cis Golgi, the site where alpha-mannosidase I has been localized. We have demonstrated this point by using 1-deoxymannojirimycin, leupeptin, and monensin. In the presence of 1-deoxymannojirimycin, a specific inhibitor of alpha-mannosidase I, differentiated HT-29 cells, as expected, accumulate Man9-8…

Proteases1-DeoxynojirimycinColonLeupeptinsCellular differentiationCellIn Vitro TechniquesBiologyBiochemistry03 medical and health sciencessymbols.namesakechemistry.chemical_compoundPolysaccharidesalpha-Mannosidase[ CHIM.ORGA ] Chemical Sciences/Organic chemistryMannosidasesTumor Cells CulturedmedicineHumansMonensinMolecular Biology030304 developmental biologychemistry.chemical_classificationGlucosamine0303 health sciencesMembrane Glycoproteins[CHIM.ORGA]Chemical Sciences/Organic chemistryEndoplasmic reticulum030302 biochemistry & molecular biologyLeupeptinBiological TransportCell DifferentiationCell BiologyCompartment (chemistry)Golgi apparatus[CHIM.ORGA] Chemical Sciences/Organic chemistrymedicine.anatomical_structureBiochemistrychemistryColonic NeoplasmssymbolsGlycoproteinProtein Processing Post-Translational
researchProduct

Pore-forming toxins trigger shedding of receptors for interleukin 6 and lipopolysaccharide.

1996

Cleavage of membrane-associated proteins with the release of biologically active macromolecules is an emerging theme in biology. However, little is known about the nature and regulation of the involved proteases or about the physiological inducers of the shedding process. We here report that rapid and massive shedding of the interleukin 6 receptor (IL-6R) and the lipopolysaccharide receptor (CD14) occurs from primary and transfected cells attacked by two prototypes of pore-forming bacterial toxins, streptolysin O and Escherichia coli hemolysin. Shedding is not induced by an streptolysin O toxin mutant which retains cell binding capacity but lacks pore-forming activity. The toxin-dependent c…

ProteasesCD14Lipopolysaccharide ReceptorsEnzyme-Linked Immunosorbent AssayBiologyTransfectionHemolysin ProteinsMonocytesCell LineHemolysin ProteinsBacterial ProteinsAntigens CDChlorocebus aethiopsEscherichia coliTumor Cells CulturedAnimalsHumansEnzyme InhibitorsReceptorCells CulturedMultidisciplinaryHaptoglobinsMacrophagesReceptors InterleukinTransfectionStaurosporineReceptors Interleukin-6Recombinant ProteinsKineticsBiochemistryStreptolysinsInterleukin-6 receptorTetradecanoylphorbol AcetateStreptolysinSignal transductionSignal TransductionResearch ArticleProceedings of the National Academy of Sciences
researchProduct

Analysis of the MHC Class I Antigen Presentation Machinery in Human Embryonal Carcinomas: Evidence for Deficiencies in TAP, LMP and MHC Class I Expre…

1998

The expression of the major histocompatibility complex (MHC) class I antigens is suppressed in early post-implantation embryonic cells as well as in embryonal carcinoma (EC) cells, but could be upregulated by treatment with interferon (IFN)-gamma or retinoic acid. In a number of human and murine tumours, defects in the expression of the different components of the MHC class I antigen processing machinery, such as the proteasomal subunits LMP-2 and LMP-7 and the peptide transporters TAP-1 and TAP-2, account for impaired MHC class I surface expression. Here, we analysed the constitutive and IFN-gamma regulated mRNA and protein expression of the LMP, TAP and MHC class I molecules in the human …

Proteasome Endopeptidase ComplexCD74HIV AntigensImmunologyCD1CytomegalovirusInterferon-gammaATP Binding Cassette Transporter Subfamily B Member 3Multienzyme ComplexesCarcinoma EmbryonalMHC class ITumor Cells CulturedHumansATP Binding Cassette Transporter Subfamily B Member 2Antigens ViralAntigen PresentationbiologyAntigen processingMHC class I antigenHistocompatibility Antigens Class ITemperatureGeneral MedicineTransporter associated with antigen processingMHC restrictionMolecular biologyUp-RegulationCysteine EndopeptidasesProtein Biosynthesisbiology.proteinATP-Binding Cassette TransportersPeptidesCD8Scandinavian Journal of Immunology
researchProduct