Search results for "TUMOR CELLS"

showing 10 items of 663 documents

Re-expression of C/EBP alpha induces CYP2B6, CYP2C9 and CYP2D6 genes in HepG2 cells.

1998

Cytochrome P450 (CYP) activity is very low or even absent in human hepatomas, a phenomenon that is accompanied by low levels of some liver transcription factors, notably C/EBP alpha. To investigate a possible link between this transcription factor and hepatic CYP expression, we have stably transfected HepG2 cells with a C/EBP alpha vector containing a Zn-inducible metallothionein promoter. Expression of functional C/EBP alpha up to liver levels concomitantly increased the mRNAs of several members of the CYP2 family (2B6, 2C9 and 2D6), suggesting that this transcription factor may play a relevant role in controlling the hepatic expression of CYP enzymes.

Carcinoma HepatocellularCYP2B6BiophysicsHepG2 cellTransfectionBiochemistryGene Expression Regulation EnzymologicCytochrome P-450 Enzyme SystemStructural BiologyTumor Cells CulturedGeneticsHumansMetallothioneinRNA MessengerVector (molecular biology)Molecular BiologyTranscription factorGeneCells CulturedCytochrome P-450 CYP2C9biologyChemistryNuclear ProteinsCytochrome P450Oxidoreductases N-DemethylatingCell BiologyTransfectionMolecular biologyDNA-Binding ProteinsCytochrome P-450 CYP2B6C/EBPαCytochrome P-450 CYP2D6Steroid 16-alpha-HydroxylaseHepatocyte nuclear factor 4 alphaEnzyme InductionSteroid HydroxylasesCCAAT-Enhancer-Binding Proteinsbiology.proteinAryl Hydrocarbon HydroxylasesHuman hepatocyteCytochrome P450 gene regulationTranscription Factors
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Development and application of test methods for the detection of dietary constituents which protect against heterocyclic aromatic amines

2003

This article describes the development and use of assay models in vitro (genotoxicity assay with genetically engineered cells and human hepatoma (HepG2) cells) and in vivo (genotoxicity and short-term carcinogenicity assays with rodents) for the identification of dietary constituents which protect against the genotoxic and carcinogenic effects of heterocyclic aromatic amines (HAs). The use of genetically engineered cells expressing enzymes responsible for the bioactivation of HAs enables the detection of dietary factors that inhibit the metabolic activation of HAs. Human derived hepatoma (HepG2) cells are sensitive towards HAs and express several enzymes [glutathione S-transferase (GST), N-…

Carcinoma HepatocellularDNA damage[SDV]Life Sciences [q-bio]Health Toxicology and Mutagenesismedicine.disease_causeIsozyme03 medical and health sciences0302 clinical medicineANTICARCINOGENEHeterocyclic CompoundsIn vivoTumor Cells CulturedGeneticsmedicineAnticarcinogenic AgentsHumansMolecular BiologyAnticarcinogenComputingMilieux_MISCELLANEOUSCarcinogen030304 developmental biologychemistry.chemical_classification0303 health sciencesChemistryLiver NeoplasmsCANCERIn vitroDietEFFET PROTECTEUREnzymeBiochemistry030220 oncology & carcinogenesisColonic NeoplasmsFood AnalysisGenotoxicityMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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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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Use of HepG2 cell line for direct or indirect mutagens screening: comparative investigation between comet and micronucleus assays.

2003

International audience; In the present study, DNA-damage and clastogenic or aneugenic effects of genotoxic compounds were examined in a metabolically competent human cell line (HepG2 cells) using the micronucleus and the comet assays. Compounds with various action mechanisms were tested: direct mutagens such as 4-nitroquinoline-N-oxide (4-NQO) and methyl methanesulfonate (MMS) and indirect mutagens requiring biotransformation to be active such as N-nitrosodimethylamine (NDMA), benzo[a]pyrene (B[a]P) and 2-acetylaminofluorene (2-AAF). The compounds were first tested for cytotoxicity by measuring their effects on RNA synthesis inhibition in HepG2 cells. 4-NQO, B[a]P and 2-AAF were the most po…

Carcinoma HepatocellularNitrosaminesHealth Toxicology and Mutagenesis[SDV]Life Sciences [q-bio]Mutagen[SDV.TOX.TCA]Life Sciences [q-bio]/Toxicology/Toxicology and food chain010501 environmental sciencesQuinolonesmedicine.disease_cause01 natural sciencesSensitivity and SpecificityDimethylnitrosamine03 medical and health sciencesClastogenchemistry.chemical_compoundInhibitory Concentration 50GeneticsmedicineBenzo(a)pyreneTumor Cells CulturedHumansCytotoxicityComputingMilieux_MISCELLANEOUS030304 developmental biology0105 earth and related environmental sciencesGenetics0303 health sciencesMicronucleus TestsChemistryLiver Neoplasms2-AcetylaminofluoreneMethyl MethanesulfonateMolecular biology4-Nitroquinoline-1-oxideMethyl methanesulfonateComet assay[SDV] Life Sciences [q-bio]Micronucleus testComet AssayMicronucleusGenotoxicityMutagensMutation research
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Immunoadhesins of interleukin-6 and the IL-6/soluble IL-6R fusion protein hyper-IL-6.

1999

Signal transduction in response to interleukin-6 (IL-6) results from homodimerization of gp130. This dimerization occurs after binding of IL-6 to its surface receptor (IL-6R) and can also be triggered by the complex of soluble IL-6R and IL-6. We fused IL-6 to the constant region of a human IgG1 heavy chain (Fc). IL-6Fc was expressed in COS-7 cells and purified via Protein A Sepharose. Using three different assays we found that the biological activity of this dimeric IL-6 protein is comparable with monomeric IL-6. Recently, we described the designer cytokine Hyper-IL-6 (H-IL-6) in which soluble IL-6R and IL-6 are connected via a flexible peptide linker. This molecule turned out to be 100-100…

Carcinoma HepatocellularRecombinant Fusion ProteinsImmunologyBiologyProtein EngineeringMiceTumor Cells CulturedImmunology and AllergyAnimalsHumansReceptorCOS cellsInterleukin-6HydrolysisThrombinBiological activityProtein engineeringGlycoprotein 130Fusion proteinReceptors Interleukin-6In vitroImmunoglobulin Fc FragmentsBiochemistryImmunoglobulin GCOS CellsSignal transductionImmunoglobulin Heavy ChainsDimerizationJournal of immunological methods
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A bioactive designer cytokine for human hematopoietic progenitor cell expansion

1997

Efficient expansion of hematopoietic progenitor cells requires, at least, the simultaneous stimulation of the receptors c-kit and gp130. While c-kit is activated by SCF; gp130, in cells which do not express sufficient amounts of IL-6R, can be activated by the complex of soluble IL-6R (sIL-6R) and IL-6. The therapeutic use of IL-6/sIL-6R, however, has been hampered by the high concentrations of the sIL-6R protein required. We have designed a fusion protein of sIL-6R and IL-6, linked by a flexible peptide chain, that was expressed to high levels. On gp130 expressing cells the fusion protein turned out to be fully active at 100 to 1,000-fold lower concentration than the combination of unlinked…

Carcinoma HepatocellularRecombinant Fusion Proteinsmedicine.medical_treatmentBiomedical EngineeringAntigens CD34BioengineeringBiologyApplied Microbiology and BiotechnologyProtein Structure SecondaryColony-Forming Units AssayAntigens CDTumor Cells CulturedmedicineHumansAmino Acid SequenceReceptorCells CulturedInterleukin 3Interleukin-6Cell growthLiver NeoplasmsReceptors InterleukinHematopoietic Stem CellsGlycoprotein 130Receptors Interleukin-6Fusion proteinCell biologyModels StructuralCytokineDrug DesignImmunologyCytokinesMolecular MedicineStem cellCell DivisionEx vivoBiotechnologyNature Biotechnology
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Stimulation of peroxisomal palmitoyl-CoA oxidase activity by ciprofibrate in hepatic cell lines: comparative studies in Fao, MH1C1 and HepG2 cells.

1993

The response of two rat cell lines, Fao and MH1C1, and one human cell line, HepG2, to the peroxisome proliferator ciprofibrate, was studied. Using a fluorometric assay for palmitoyl-CoA oxidase, the dose- and time-dependent increase of this enzymatic activity was determined. From the lowest concentration (100 microM) stimulation is evident in the two rat cell lines. In the Fao line, the activity was stimulated reaching a seven-fold increase over the control level at 250 microM after 72 h of treatment. In the MH1C1 line, the maximum stimulation, four- to five-fold, was obtained at 250 and 500 microM after 72 h. In the HepG2 cell line, activity increased two-fold at 250 microM after 72 h reac…

Carcinoma HepatocellularStimulationBiologyMicrobodiesClofibric AcidLiver Neoplasms ExperimentalmedicineTumor Cells CulturedAcyl-CoA oxidaseAnimalsHumansHypolipidemic AgentsOxidase testLiver NeoplasmsFibric AcidsCell BiologyGeneral MedicinePeroxisomePalmitoyl-CoA oxidase activityBiochemistryLiverCell cultureHepatic stellate cellCiprofibrateOxidoreductasesmedicine.drugBiology of the cell
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Novel cell culture systems for the hepatitis C virus.

2001

Infections with the hepatitis C virus (HCV) are a major cause of acute and chronic liver disease. The high prevalence of the virus, the insidious course of the disease and the poor prognosis for long-term persistent infection make this pathogen a serious medical and socioeconomical problem. The identification of the viral genome approximately 10 years ago rapidly led to the delineation of the genomic organization and the structural and biochemical characterization of several virus proteins. However, studies of the viral life cycle as well as the development of antiviral drugs have been difficult because of the lack of a robust and reliable cell culture system. Numerous attempts have been un…

Carcinoma HepatocellularVirus CultivationvirusesHepacivirusHepatitis C virusGenome ViralHepacivirusmedicine.disease_causeTransfectionVirus ReplicationVirusFlaviviridaeViral life cycleVirologymedicineTumor Cells CulturedAnimalsHumansCells CulturedPharmacologybiologyLiver Neoplasmsbiology.organism_classificationVirologyViral replicationCell cultureDrug DesignImmunologyRepliconViral diseaseAntiviral research
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Replication of subgenomic hepatitis C virus RNAs in a hepatoma cell line.

1999

An estimated 170 million persons worldwide are infected with hepatitis C virus (HCV), a major cause of chronic liver disease. Despite increasing knowledge of genome structure and individual viral proteins, studies on virus replication and pathogenesis have been hampered by the lack of reliable and efficient cell culture systems. A full-length consensus genome was cloned from viral RNA isolated from an infected human liver and used to construct subgenomic selectable replicons. Upon transfection into a human hepatoma cell line, these RNAs were found to replicate to high levels, permitting metabolic radiolabeling of viral RNA and proteins. This work defines the structure of HCV replicons funct…

Carcinoma HepatocellularVirus CultivationvirusesHepatitis C virusDrug ResistanceGenome ViralHepacivirusBiologyViral Nonstructural Proteinsmedicine.disease_causeTransfectionVirus ReplicationViruschemistry.chemical_compoundmedicineTumor Cells CulturedHumansCloning MolecularNS5ANS5BSubgenomic mRNAGeneticsNS3MultidisciplinaryLiver NeoplasmsVirologyHepatitis CNS2-3 proteaseViral replicationchemistryRNA ViralRepliconGentamicinsScience (New York, N.Y.)
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Toxicity of waste gasification bottom ash leachate

2011

Abstract Toxicity of waste gasification bottom ash leachate from landfill lysimeters (112 m3) was studied over three years. The leachate of grate incineration bottom ash from a parallel setup was used as reference material. Three aquatic organisms (bioluminescent bacteria, green algae and water flea) were used to study acute toxicity. In addition, an ethoxyresorufin-O-deethylase (EROD) assay was performed with mouse hepatoma cells to indicate the presence of organic contaminants. Concentrations of 14 elements and 15 PAH compounds were determined to characterise leachate. Gasification ash leachate had a high pH (9.2–12.4) and assays with and without pH adjustment to neutral were used. Gasifi…

Carcinoma Hepatocellularanimal diseasesta1172Coal AshMiceAlgaeChlorophytaToxicity TestsCytochrome P-450 CYP1A1Tumor Cells CulturedAnimalsLeachateWaste Management and DisposalWaste managementbiologyChemistryLiver Neoplasmstechnology industry and agricultureContaminationbiology.organism_classificationAliivibrio fischeriAcute toxicityRefuse DisposalIncinerationEnzyme ActivationDaphniaBottom ashLysimeterEnvironmental chemistryLuminescent MeasurementsGreen algaeWater Pollutants ChemicalWaste Management
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