Search results for "5-Azacytidine"

showing 4 items of 4 documents

The DNA methylation inhibitor 5-azacytidine modulates 6-thioguanine toxicity in mammalian cells

2003

In order to assess the effects of combining two antimetabolites used separately to treat human leukemias, we carried out an experimental study by exposing V79 Chinese hamster cells, a 6-thioguanine (6-tG)-sensitive cell line, to sequential and concurrent treatments with 5-azacytidine (5-azaC) and 6-tG. In this paper, we demonstrate that there is a clear dependency for the way in which this combination was tested. Pre-treatment with 5-azaC made V79 cells more resistant to 6-tG by a substantial reduction in 6-tG incorporation into DNA; this effect could still be detected for several cell divisions after the removal of 5-azaC, and was achieved neither by reduced cell growth nor by the inductio…

Antimetabolites AntineoplasticHypoxanthine Phosphoribosyltransferasemedicine.drug_classCell SurvivalCellHamsterToxicologyAntimetaboliteChinese hamster6-thioguanineCricetulus5-azacytidineCricetinaeAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsThioguanineCells CulturedbiologyCell growthtoxicityDrug SynergismGeneral MedicineDNAProdrugDNA Methylationbiology.organism_classificationMolecular biologySettore BIO/18 - Geneticamedicine.anatomical_structureBiochemistryCell cultureToxicityAzacitidineSister Chromatid ExchangeCell Division
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Role and importance of polymorphisms with respect to DNA methylation for the expression of CYP2E1 enzyme

2014

Different individuals possess slightly different genetic information and show genetically-determined differences in several enzyme activities due to genetic variability. Following an integrated approach, we studied the polymorphisms and methylation of sites contained in the 5' flanking region of the metabolizing enzyme CYP2E1 in correlation to its expression in both tumor and non-neoplastic liver cell lines, since to date little is known about the influence of these (epi)genetic elements in basal conditions and under induction by the specific inductor and a demethylating agent. In treated cells, reduced DNA methylation, assessed both at genomic and gene level, was not consistently associate…

Genotype5' Flanking RegionCell Survival5' flanking regionMinisatellite RepeatsBiologyGene Expression Regulation EnzymologicGenotypeGeneticsCYP2E1 gene polymorphismTumor Cells CulturedHumansGeneHepatocellular carcinoma cell lines; CYP2E1 gene polymorphisms; DNA methylation; 5-Azacytidine; Ethanol;GeneticsPolymorphism GeneticEthanolLiver cellHaplotype5-AzacytidineCytochrome P-450 CYP2E1General MedicineMethylationHep G2 CellsHepatocellular carcinoma cell lineDNA MethylationMolecular biologySettore BIO/18 - GeneticaDNA methylationAzacitidineRestriction fragment length polymorphismPolymorphism Restriction Fragment Length
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Promoter methylation of MGMT, MLH1 and RASSF1A tumor suppressor genes in head and neck squamous cell carcinoma: Pharmacological genome demethylation …

2012

Promoter hypermethylation of tumor suppressor genes (TSGs) is a common feature of primary cancer cells. However, to date the somatic epigenetic events that occur in head and neck squamous cell carcinoma (HNSCC) tumorigenesis have not been well-defined. In the present study, we analyzed the promoter methylation status of the genes mutL homolog 1 (MLH1), Ras-association domain family member 1 (RASSF1A) and O-6-methylguanine-DNA methyltransferase (MGMT) in 23 HNSCC samples, three control tissues and one HNSCC cell line (UM-SCC 33) using methylation-specific PCR (MSP). The expression of the three proteins was quantified by semi-quantitative immunohistochemical analysis. The cell line was treate…

MaleCancer Researchmedicine.disease_causePolymerase Chain Reactionchemistry.chemical_compoundRas association domain family member 1Genes Tumor Suppressortumor suppressor geneEnzyme InhibitorsPromoter Regions GeneticDNA Modification MethylasesAged 80 and overNuclear ProteinsArticlesGeneral MedicineMethylationMiddle AgedImmunohistochemistryPrimary tumorOncologyDealkylationHead and Neck NeoplasmsDNA methylationAzacitidineCarcinoma Squamous CellFemaleMutL Protein Homolog 1Molecular Sequence DataDown-RegulationBiologyhead and neck squamous cell carcinomamutL homolog 15-azacytidineCell Line TumormedicineHumansEpigeneticsneoplasmsO-6-methylguanine-DNA methyltransferaseAdaptor Proteins Signal TransducingAgedCell ProliferationBase SequenceDose-Response Relationship DrugTumor Suppressor ProteinsSequence Analysis DNADNA Methylationmedicine.diseaseHead and neck squamous-cell carcinomaMolecular biologyDemethylating agentSquamous carcinomastomatognathic diseasesDNA Repair EnzymeschemistryCase-Control StudiesCpG IslandsCarcinogenesisOncology Reports
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5-Azacytidine Inhibits the Activation of Senescence Program and Promotes Cytotoxic Autophagy during Trdmt1-Mediated Oxidative Stress Response in Insu…

2022

5-Azacytidine (5-azaC), a methyltransferase inhibitor and anticancer drug, can promote several cellular stress responses such as apoptosis, autophagy, and senescence. The action of 5-azaC is complex and can be modulated by dose, time of treatment, and co-administration with oxidants. Insulinoma is a rare pancreatic neuroendocrine tumor with limited chemotherapeutic options. In the present study, two cellular models of insulinoma were considered, namely NIT-1 and β-TC-6 mouse cells, to evaluate the effects of 5-azaC post-treatment during hydrogen peroxide-induced oxidative stress. 5-azaC attenuated the development of oxidant-induced senescent phenotype in both cell lines. No pro-apoptotic ac…

autophagyAntineoplastic AgentsMethyltransferasesGeneral MedicineinsulinomaOxidantsPancreatic NeoplasmsMiceOxidative Stress5-azacytidinenitric oxideSettore BIO/10 - BiochimicaAzacitidineAnimalsCells
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