Search results for "Hep G2"

showing 10 items of 121 documents

Transcriptomic responses generated by hepatocarcinogens in a battery of liver-based in vitro models

2013

As the conventional approach to assess the potential of a chemical to cause cancer in humans still includes the 2-year rodent carcinogenicity bioassay, development of alternative methodologies is needed. In the present study, the transcriptomics responses following exposure to genotoxic (GTX) and non-genotoxic (NGTX) hepatocarcinogens and non-carcinogens (NC) in five liver-based in vitro models, namely conventional and epigenetically stabilized cultures of primary rat hepatocytes, the human hepatoma-derived cell lines HepaRG and HepG2 and human embryonic stem cell-derived hepatocyte-like cells, are examined. For full characterization of the systems, several bioinformatics approaches are emp…

Cancer ResearchGene Expressiongene expression profilingComputational biologyBiologyPharmacologyTranscriptomeRats Sprague-Dawley03 medical and health sciences0302 clinical medicineCell Line TumorBioassayAnimalsHumansGeneCarcinogenEmbryonic Stem Cells030304 developmental biology0303 health sciencesGene Expression ProfilingLiver Neoplasmspathwaysbased analysis liver-based in vitro modelGeneral MedicineHep G2 CellsEmbryonic stem cellIn vitro3. Good healthRatsgenotoxic carcinogens non-genotoxic carcinogensGene expression profilingLiverCell culture030220 oncology & carcinogenesisCarcinogensHepatocytesTumor Suppressor Protein p53TranscriptomeMutagens
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Chemotherapy-induced apoptosis in hepatocellular carcinoma involves the p53 family and is mediatedviathe extrinsic and the intrinsic pathway

2010

We investigated the downstream mechanisms by which chemotherapeutic drugs elicit apoptosis in hepatocellular carcinoma (HCC). Genomic signatures of HCC cell lines treated with different chemotherapeutic drugs were obtained. Analyses of apoptosis pathways were performed and RNA interference was used to evaluate the role of the p53 family. Endogenous p53, p63 and p73 were upregulated in response to DNA damage by chemotherapeutic drugs. Blocking p53 family function led to chemoresistance in HCC. Stimulation and blocking experiments of the CD95-, the TNF- and the TRAIL-receptor systems revealed that cytotoxic drugs, via the p53 family members as transactivators, can trigger expression of each o…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTumor suppressor geneDNA damagetumor suppressor protein p53membrane proteinsoligonucleotide array sequence analysiscarcinomaBiologyhepatocellularfas-associated death domain proteinAPAF1humansMembrane Potential Mitochondrialhep G2 cellsbleomycinliver neoplasmsSettore BIO/11apoptosisPrognosismitochondrialFas receptorcaspasesOncologyApoptosisbiology.proteinCancer researchMdm2membrane potentialSignal transductionPrognosis; bleomycin; caspases; membrane potential mitochondrial; oligonucleotide array sequence analysis; tumor suppressor protein p53; membrane proteins; fas-associated death domain protein; humans; liver neoplasms; hep G2 cells; apoptosis; carcinoma hepatocellularInternational Journal of Cancer
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Aspidin PB, a phloroglucinol derivative, induces apoptosis in human hepatocarcinoma HepG2 cells by modulating PI3K/Akt/GSK3β pathway.

2012

Aspidin PB, a phloroglucinol derivative isolated from Dryopteris fragrans (L.) Schott, has been previously reported to exert high biological activities. In the present study, we analyzed the apoptotic mechanisms of aspidin PB on human hepatoma cell line, HepG2. Initially, aspidin PB was shown to inhibit the growth of HepG2 cells in a time and dose-dependent manner. After treatment with aspidin PB for 72 h, 48 h and 24 h using MTT assay, the IC(50) values were 10.59 μM, 20.86 μM and 46.59 μM, respectively. Aspidin PB was capable to induce apoptosis, as measured by mitochondrial membrane potential (ΔΨm), acridine orange (AO) staining and propidium iodide (PI)/annexin V-FITC double staining. T…

Carcinoma HepatocellularApoptosisBiologyPhloroglucinolToxicologyWortmanninchemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesAnnexinHumansMTT assayPropidium iodideProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationPhosphoinositide-3 Kinase InhibitorsMembrane Potential MitochondrialGlycogen Synthase Kinase 3 betaMicroscopy ConfocalAcridine orangeLiver NeoplasmsGeneral MedicineHep G2 CellsFlow CytometryMolecular biologyAndrostadieneschemistryApoptosisWortmanninProto-Oncogene Proteins c-aktSignal TransductionChemico-biological interactions
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Analysis of Possible Mechanisms Accounting for Raf-1 Kinase Inhibitor Protein Downregulation in Hepatocellular Carcinoma

2012

Abstract Raf-1 kinase inhibitor protein (RKIP) is a tumor and metastasis suppressor that promotes drug-induced apoptosis in cancer cells. It is frequently downregulated, both at the mRNA and protein level, in hepatocellular carcinoma (HCC), but the mechanisms leading to this reduction are obscure. We sequenced the whole RKIP gene in three human HCC cell lines (HA22T/VGH, HepG2, and Hep3B), and in five clinical HCC samples, but could not find any gene variant that might account for their low RKIP levels. We also examined whether gene methylation may be responsible for the altered RKIP expression. No methylation of the RKIP gene was found in the tumor samples, while among the cell lines only …

Carcinoma HepatocellularLeupeptinsAntineoplastic AgentsPhosphatidylethanolamine Binding ProteinRKIP (Raf-1 kinase inhibitor protein) hepatocellular carcinomaBiologyBiochemistryDownregulation and upregulationRNA interferenceCell Line TumorGeneticsHumansMetastasis suppressorPromoter Regions GeneticMolecular BiologyRegulation of gene expressionKinaseLiver NeoplasmsHep G2 CellsMethylationDNA Methylationdigestive system diseasesGene Expression Regulation NeoplasticMicroRNAsMutationCancer cellDNA methylationAzacitidineSettore BIO/14 - FarmacologiaCancer researchMolecular MedicineRNA InterferenceBiotechnologyOMICS: A Journal of Integrative Biology
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Cytotoxic effects and degradation products of three mycotoxins: Alternariol, 3-acetyl-deoxynivalenol and 15-acetyl-deoxynivalenol in liver hepatocell…

2015

This work is focused in studying the cytotoxic effects on HepG2 cells of the mycotoxins alternariol (AOH), 3-acetyl-deoxynivalenol (3-ADON) and 15-acetyl-deoxynivalenol (15-ADON) by the MTT assay, as well as in the identification of the degradation products and/or metabolites originated after treatment by liquid chromatography tandem mass spectrometry (LC-MS/MS) equipment and extracted from culture media. HepG2 cells were treated at different concentrations over 24, 48 and 72 h. The IC50 values were from 65 to 96 μM, from 3.6 to 6.2 μM and from 5.2 to 8.1 μM for AOH, 3-ADON and 15-ADON, respectively. Among all three mycotoxins assayed, deoxynivalenol (DON) derivated presented the highest to…

Carcinoma HepatocellularTime FactorsCell SurvivalAlternariolToxicologyMass spectrometryInhibitory Concentration 50Lactoneschemistry.chemical_compoundTandem Mass SpectrometryLiquid chromatography–mass spectrometryHumansMTT assayCysteineMycotoxinBiotransformationChromatography Reverse-PhaseChromatographyDose-Response Relationship DrugLiver NeoplasmsHep G2 CellsGeneral MedicineGlutathioneSulfuric AcidsGlutathionechemistryTrichothecenesConjugateCysteineToxicology Letters
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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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High-content imaging technology for the evaluation of drug-induced steatosis using a multiparametric cell-based assay.

2012

In the present study, we developed a cell-based protocol for the identification of drugs able to induce steatosis. The assay measures multiple markers of toxicity in a 96-well plate format using high-content screening (HCS) technology. After treating HepG2 cells with increasing concentrations of the tested compounds, toxicity parameters were analyzed using fluorescent probes: BODIPY493/503 (lipid content), 2',7'-dihydrodichlorofluorescein diacetate (reactive oxygen species [ROS] generation), tetramethyl rhodamine methyl ester (mitochondrial membrane potential), propidium iodide (cell viability), and Hoechst 33342 (nuclei staining). A total of 16 drugs previously reported to induce liver ste…

Cell SurvivalCellDrug Evaluation PreclinicalBiologyBiochemistryAnalytical ChemistryCell Linechemistry.chemical_compoundmedicineHumansPropidium iodideViability assayFluorescent Dyeschemistry.chemical_classificationReactive oxygen speciesHep G2 Cellsmedicine.diseaseMolecular biologyStainingFatty Livermedicine.anatomical_structurechemistryLiverMicroscopy FluorescenceHigh-content screeningToxicityMolecular MedicineSteatosisReactive Oxygen SpeciesBiomarkersBiotechnologyJournal of biomolecular screening
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Interactions between T-2 toxin and its metabolites in HepG2 cells and in silico approach

2021

Abstract The T-2 toxin (T-2) is commonly metabolized to HT-2 toxin (HT-2), Neosolaniol (NEO), T2-triol and T2-tetraol and they can modify the toxicity of T-2. In this study, T-2 and its modified forms were evaluated by in vitro and in silico methods. The in vitro cytotoxicity individually was evaluated by MTT and Total Protein Content (PC) assays in human hepatocarcinoma (HepG2) cells. The order of IC50 was T-2 tetraol > T-2 triol > NEO > T-2 = HT-2. The T-2 and HT-2 evidenced the highest cytotoxic effect in HepG2 cells individually. No differences were observed in binary combinations tested and the two mycotoxins in the mixture tested individually. The T-2+HT-2 combination showed the highe…

Cell SurvivalIn silicoToxicologymedicine.disease_cause03 medical and health sciences0404 agricultural biotechnologymedicineHumansCytotoxic T cellComputer SimulationCytotoxicityIC50030304 developmental biologyADME0303 health sciencesDose-Response Relationship DrugToxinChemistryHep G2 Cells04 agricultural and veterinary sciencesGeneral Medicine040401 food scienceIn vitroT-2 ToxinBiochemistryToxicityFood ScienceFood and Chemical Toxicology
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Multiparametric evaluation of the cytoprotective effect of the Mangifera indica L. stem bark extract and mangiferin in HepG2 cells.

2012

Abstract Objective Mango (Mangifera indica L.) stem bark extract (MSBE) is a natural product with biological properties and mangiferin is the major component. This paper reported the evaluation of the protective effects of MSBE and mangiferin against the toxicity induced in HepG2 cells by tert-butyl hydroperoxide or amiodarone. Method Nuclear morphology, cell viability, intracellular calcium concentration and reactive oxygen species (ROS) production were measured by using a high-content screening multiparametric assay. Key findings MSBE and mangiferin produced no toxicity below 500 mg/ml doses. A marked recovery in cell viability, which was reduced by the toxicants, was observed in cells pr…

Cell SurvivalXanthonesPharmaceutical ScienceAmiodaronePharmacologychemistry.chemical_compoundtert-ButylhydroperoxidemedicineHumansMangiferaViability assayATP Binding Cassette Transporter Subfamily B Member 1MangiferinP-glycoproteinPharmacologychemistry.chemical_classificationReactive oxygen speciesMangiferabiologyDose-Response Relationship DrugPlant StemsPlant ExtractsHep G2 Cellsmedicine.diseaseCytoprotectionMitochondrial toxicityBiochemistrychemistryToxicitybiology.proteinPlant BarkCalciumReactive Oxygen SpeciesThe Journal of pharmacy and pharmacology
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Changes in carnitine octanoyltransferase activity induce alteration in fatty acid metabolism

2011

The peroxisomal beta oxidation of very long chain fatty acids (VLCFA) leads to the formation of medium chain acyl-CoAs such as octanoyl-CoA. Today, it seems clear that the exit of shortened fatty acids produced by the peroxisomal beta oxidation requires their conversion into acyl-carnitine and the presence of the carnitine octanoyltransferase (CROT). Here, we describe the consequences of an overexpression and a knock down of the CROT gene in terms of mitochondrial and peroxisomal fatty acids metabolism in a model of hepatic cells. Our experiments showed that an increase in CROT activity induced a decrease in MCFA and VLCFA levels in the cell. These changes are accompanied by an increase in …

CellBiophysicsOxidative phosphorylationBiochemistrychemistry.chemical_compoundPeroxisomesmedicineHumansCarnitineRNA Small InterferingMolecular Biologychemistry.chemical_classificationFatty acid metabolismFatty AcidsHep G2 CellsCell BiologyMetabolismPeroxisomeHEK293 Cellsmedicine.anatomical_structureEnzymeCarnitine AcyltransferaseschemistryBiochemistryGene Knockdown TechniquesHepatic stellate cellOxidation-Reductionmedicine.drugBiochemical and Biophysical Research Communications
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