Search results for "Cell Line"

showing 10 items of 2924 documents

Antitumor Cell-Complex Vaccines Employing Genetically Modified Tumor Cells and Fibroblasts

2014

The present study evaluates the immune response mediated by vaccination with cell complexes composed of irradiated B16 tumor cells and mouse fibroblasts genetically modified to produce GM-CSF. The animals were vaccinated with free B16 cells or cell complexes. We employed two gene plasmid constructions: one high producer (pMok) and a low producer (p2F). Tumor transplant was performed by injection of B16 tumor cells. Plasma levels of total IgG and its subtypes were measured by ELISA. Tumor volumes were measured and survival curves were obtained. The study resulted in a cell complex vaccine able to stimulate the immune system to produce specific anti-tumor membrane proteins (TMP) IgG. In the g…

non-viralHealth Toxicology and MutagenesisGenetic enhancementCellMelanoma Experimentallcsh:MedicineBiologyToxicologyArticleImmunoglobulin GMicePlasmidImmune systemCell Line TumormedicineAnimalsCells Culturedlcsh:RGranulocyte-Macrophage Colony-Stimulating FactorMembrane ProteinsTransfectionFibroblastsMolecular biologygene therapycell complexesTumor BurdenGenetically modified organismGranulocyte macrophage colony-stimulating factormedicine.anatomical_structureImmunoglobulin Gbiology.proteincancer vaccinesbystander cellsmedicine.drugToxins
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Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax

2019

Experimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro‐survival and anti‐apoptotic roles through molecule phosphorylated extracellular signal‐regulated kinase1/2 (p‐ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p‐ERK1/2 and pro‐apoptotic molecule Bax. In this study, the rat‐derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the ca…

ohjelmoitunut solukuolemaBaxsydänapoptosiscardiac myocyteRap guanine nucleotide exchange factor 1proteiinithenkiinjääminenH9C2 cell linep-ERK1/2lihassolut
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3AB-OS, a human osteosarcoma stem-like cell line, potential model for studying cancer

2012

osteosarcoma stem-like cell line
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Hepatocellular cancer cell lines, Hep-3B and Hep-G2 display the pleiotropic response to resveratrol and berberine

2022

Purpose Human carcinoma cells with different p53 status exposed to a combination of bioactive substances, resveratrol and berberine, revealed different responses in cell viability via p53-dependant apoptosis pathway activation. Materials and methods Using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay, we investigated various and opposing effects in hepatocellular carcinoma cells, Hep-G2 and Hep-3B with different p53-status. Results Cells decreased in viability after treatment with dose-dependent concentrations of resveratrol and berberine. Hep-3B p53 mutants were more sensitive in comparison to the p53 wild type Hep-G2 cell line. A syne…

p53 statusViability isobologramBerberine and resveratrol treatmentsHuman hepatocellular cancer cellsHep-G2 and Hep-3B cell LinesAdvances in Medical Sciences
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Influence of aryl hydrocarbon- (Ah) receptor and genotoxins on DNA repair gene expression and cell survival of mouse hepatoma cells

2009

The aryl hydrocarbon receptor (AhR) mediates toxicity of a variety of environmental pollutants such as polycyclic aromatic hydrocarbons (PAHs) and dioxins. However, the underlying mechanisms and genetic programmes regulated by AhR to cause adverse effects but also to counteract poisoning are still poorly understood. Here we analysed the effects of two AhR ligands, benzo[a]pyrene (B[a]P), a DNA damaging tumour initiator and promotor and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a pure tumour promoter, on cell survival and on nucleotide excision repair (NER) gene expression. NER deals with so called "bulky" DNA adducts including those generated by enzymatically activated B[a]P. Therefore, t…

p53Aryl hydrocarbon receptor nuclear translocatorDNA RepairTumor suppressor geneCell SurvivalDNA damageDNA repairBlotting WesternDNA-Directed DNA Polymerasecis-PlatinBiologyToxicologyMiceLiver Neoplasms ExperimentalCell Line TumorGene expressionAnimals2378-Tetrachlorodibenzo-p-dioxinGeneAryl hydrocarbon receptorGene Expression ProfilingAryl Hydrocarbon Receptor Nuclear TranslocatorGenes p53Aryl hydrocarbon receptorMolecular biologyNucleotide excision repairBenzo[a]pyreneGene Expression RegulationReceptors Aryl HydrocarbonBiochemistrybiology.proteinEnvironmental PollutantsMutagensNucleotide excision repairToxicology
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Targeting HSP90 with the small molecule inhibitor AUY922 (luminespib) as a treatment strategy against hepatocellular carcinoma

2018

Hepatocellular carcinoma (HCC) is a highly malignant tumor that responds very poorly to existing therapies, most probably due to its extraordinary inter- and intra-tumor molecular heterogeneity. The modest therapeutic response to molecular targeted agents underlines the need for new therapeutic approaches for HCC. In our study, we took advantage of well-characterized human HCC cell lines, differing in transcriptomic subtypes, DNA mutation and amplification alterations, reflecting the heterogeneity of primary HCCs, to provide a preclinical evaluation of the specific heat shock protein 90 (HSP90) inhibitor AUY922 (luminespib). Indeed, HSP90 is highly expressed in different tumor types, but it…

p53MaleCancer ResearchCellTranscriptome0302 clinical medicineHCCbeta CateninAged 80 and overLuminespibAUY922Liver NeoplasmsHep G2 CellsSorafenibMiddle AgedUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyCaspases030220 oncology & carcinogenesisHepatocellular carcinomaFemaleNUPR1medicine.drugAdultSorafenibCarcinoma Hepatocellularβ-CateninMice NudeAntineoplastic AgentsSmall Molecule Libraries03 medical and health sciencesDownregulation and upregulationIn vivoCell Line TumormedicineHSP90AnimalsHumansHSP90 Heat-Shock ProteinsAgedCell growthbusiness.industryMcl-1IsoxazolesResorcinolsHCCSmedicine.diseasedigestive system diseasesMutationCancer researchTranscriptomebusinessInternational Journal of Cancer
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The mechanism of parthenolide-induced cell death in tumor cell lines.

2011

parthenolide cancer cell lines
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TRAIL acts synergistically with iron oxide nanocluster-mediated magneto- and photothermia

2019

International audience; Targeting TRAIL (Tumor necrosis factor (TNF)-Related Apoptosis-Inducing Ligand) receptors for cancer therapy remains challenging due to tumor cell resistance and poor preparations of TRAIL or its derivatives. Herein, to optimize its therapeutic use, TRAIL was grafted onto iron oxide nanoclusters (NCs) with the aim of increasing its pro-apoptotic potential through nanoparticle-mediated magnetic hyperthermia (MHT) or photothermia (PT). Methods: The nanovector, NC@TRAIL, was characterized in terms of size, grafting efficiency, and potential for MHT and PT. The therapeutic function was assessed on a TRAIL-resistant breast cancer cell line, MDA-MB-231, wild type (WT) or T…

photothermal therapyCell SurvivalMedicine (miscellaneous)TRAIL02 engineering and technologyFerric CompoundsFlow cytometryTNF-Related Apoptosis-Inducing LigandCell membrane03 medical and health sciences0302 clinical medicineMicroscopy Electron TransmissionCell surface receptorCell Line Tumormedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologymagnetic hyperthermiaReceptorPharmacology Toxicology and Pharmaceutics (miscellaneous)ComputingMilieux_MISCELLANEOUSchemistry.chemical_classificationCell Deathmedicine.diagnostic_testTumor Necrosis Factor-alphairon oxide nanoclustersapoptosisHyperthermia InducedFlow Cytometry021001 nanoscience & nanotechnology3. Good healthMagnetic hyperthermiamedicine.anatomical_structurechemistryTransferrinApoptosis030220 oncology & carcinogenesisCancer research[SDV.IB]Life Sciences [q-bio]/BioengineeringTumor necrosis factor alpha0210 nano-technologyResearch Paper
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Rac1 and PAK1 are upstream of IKK-ε and TBK-1 in the viral activation of interferon regulatory factor-3

2004

The anti-viral type I interferon (IFN) response is initiated by the immediate induction of IFN beta, which is mainly controlled by the IFN-regulatory factor-3 (IRF-3). The signaling pathways mediating viral IRF-3 activation are only poorly defined. We show that the Rho GTPase Rac1 is activated upon virus infection and controls IRF-3 phosphorylation and activity. Inhibition of Rac1 leads to reduced IFN beta promoter activity and to enhanced virus production. As a downstream mediator of Rac signaling towards IRF-3, we have identified the kinase p21-activated kinase (PAK1). Furthermore, both Rac1 and PAK1 regulate the recently described IRF-3 activators, I kappa B kinase- and TANK-binding kina…

rac1 GTP-Binding ProteinTranscription GeneticBiophysicsIκB kinaseProtein Serine-Threonine KinasesSignal transductionBiologyVirus ReplicationBiochemistryCell LineDogsPAK1Structural BiologyInterferonGeneticsmedicineAnimalsHumansPhosphorylationPromoter Regions Geneticp21-activated kinasesMolecular BiologyRNA Double-StrandedKinaseRho GTPaseI-Kappa-B KinaseNuclear ProteinsInterferon-betaCell BiologyCREB-Binding ProteinI-kappa B KinaseDNA-Binding ProteinsEnzyme Activationp21-Activated KinasesInfluenza A virusViral infectionAnti-viral responseTrans-ActivatorsCancer researchInterferon Regulatory Factor-3Transcription factorSignal transductionDimerizationTranscription FactorsInterferon regulatory factorsmedicine.drugFEBS Letters
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Rac1 protein signaling is required for DNA damage response stimulated by topoisomerase II poisons.

2012

To investigate the potency of the topoisomerase II (topo II) poisons doxorubicin and etoposide to stimulate the DNA damage response (DDR), S139 phosphorylation of histone H2AX (γH2AX) was analyzed using rat cardiomyoblast cells (H9c2). Etoposide caused a dose-dependent increase in the γH2AX level as shown by Western blotting. By contrast, the doxorubicin response was bell-shaped with high doses failing to increase H2AX phosphorylation. Identical results were obtained by immunohistochemical analysis of γH2AX focus formation, comet assay-based DNA strand break analysis, and measuring the formation of the topo II-DNA cleavable complex. At low dose, doxorubicin activated ataxia telangiectasia m…

rac1 GTP-Binding Proteinrho GTP-Binding ProteinsDNA damageAntineoplastic AgentsBiochemistryPoisonsCell LineHistonesNeoplasmsmedicineAnimalsTopoisomerase II InhibitorsDoxorubicinMolecular BiologyEtoposidebiologyCell DeathTopoisomeraseCell BiologyMolecular biologyImmunohistochemistryRatsComet assayHistoneDNA Topoisomerases Type IIDNA Topoisomerases Type Ibiology.proteinPhosphorylationTopoisomerase-II InhibitorHydroxymethylglutaryl-CoA Reductase Inhibitorsmedicine.drugDNA DamageSignal TransductionThe Journal of biological chemistry
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