Search results for "Histone Deacetylase Inhibitors"

showing 5 items of 55 documents

Role of hepatocyte nuclear factor 3γ in the expression of human CYP2C genes

2004

Hepatocyte nuclear factor 3 gamma (HNF-3 gamma) is an important transcription factor for the maintenance of specific liver functions. However, its relevance in the expression of human cytochrome P450 (CYP) genes has not yet been explored. Several HNF3 putative binding sites can be identified in human CYP2C 5'-flanking regions. Gene reporter experiments with proximal promoters revealed that HNF-3 gamma transactivated CYP2C8, CYP2C9, and CYP2C19 (25-, 4-, and 4-fold, respectively), but it did not transactivate CYP2C18. However, overexpression of HNF-3 gamma in hepatoma cells by means of a recombinant adenovirus induced CYP2C9, CYP2C18, and CYP2C19 mRNA (4.5-, 20-, and 50-fold, respectively) b…

Transcriptional ActivationRecombinant Fusion ProteinsGenetic VectorsBiophysicsBiologyHydroxamic AcidsTransfectionBiochemistryGene Expression Regulation EnzymologicAdenoviridaeCytochrome P-450 Enzyme SystemSp3 transcription factorCell Line TumormedicineHumansRNA MessengerEnzyme InhibitorsLuciferasesPromoter Regions GeneticMolecular BiologyTranscription factorBinding SitesNuclear ProteinsPromoterMolecular biologyDNA-Binding ProteinsHistone Deacetylase InhibitorsHepatocyte nuclear factorsTrichostatin AHepatocyte nuclear factor 4Hepatocyte nuclear factor 4 alphaHepatocytesFOXA2Transcription Initiation SiteHepatocyte Nuclear Factor 3-gammaHeLa CellsTranscription Factorsmedicine.drugArchives of Biochemistry and Biophysics
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Transcriptional Regulation of Human CYP3A4 Basal Expression by CCAAT Enhancer-Binding Protein α and Hepatocyte Nuclear Factor-3γ

2003

Cytochrome P450 3A4 (CYP3A4) is involved in the metabolism of more than 50% of currently used therapeutic drugs, yet the mechanisms that control CYP3A4 basal expression in liver are poorly understood. Several putative binding sites for CCAAT/enhancer-binding protein (C/EBP) and hepatic nuclear factor 3 (HNF-3) were found by computer analysis in CYP3A4 promoter. The use of reporter gene assays, electrophoretic mobility shift assays, and site-directed mutagenesis revealed that one proximal and two distal C/EBP alpha binding sites are essential sites for the trans-activation of CYP3A4 promoter. No trans-activation was found in similar reporter gene experiments with a HNF-3 gamma expression vec…

Transcriptional ActivationTranscription GeneticGenetic VectorsBiologyTransfectiondigestive systemGene Expression Regulation EnzymologicChromatin remodelingAdenoviridaeCytochrome P-450 Enzyme SystemCCAAT-Enhancer-Binding Protein-alphamedicineCytochrome P-450 CYP3AHumansEnzyme InhibitorsBinding sitePromoter Regions GeneticCells CulturedPharmacologyReporter geneExpression vectorCcaat-enhancer-binding proteinsNuclear ProteinsMolecular biologyChromatinDNA-Binding ProteinsHistone Deacetylase InhibitorsHepatocyte nuclear factorsTrichostatin AHepatocytesMolecular MedicineHepatocyte Nuclear Factor 3-gammaTranscription Factorsmedicine.drugMolecular Pharmacology
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Pleiotropic antitumor effects of the pan-HDAC inhibitor ITF2357 against c-Myc-overexpressing human B-cell non-Hodgkin lymphomas,

2014

Histone deacetylases (HDAC) extensively contribute to the c-Myc oncogenic program, pointing to their inhibition as an effective strategy against c-Myc-overexpressing cancers. We, thus, studied the therapeutic activity of the new-generation pan-HDAC inhibitor ITF2357 (Givinostat®) against c-Myc-overexpressing human B-cell non-Hodgkin lymphomas (B-NHLs). ITF2357 anti-proliferative and pro-apoptotic effects were analyzed in B-NHL cell lines with c-Myc translocations (Namalwa, Raji and DOHH-2), stabilizing mutations (Raji) or post-transcriptional alterations (SU-DHL-4) in relationship to c-Myc modulation. ITF2357 significantly delayed the in vitro growth of all B-NHL cell lines by inducing G1 c…

c-MycmicroRNAnon-Hodgkin lymphomac-Myc; histone deacetylase inhibitors; microRNA; non-Hodgkin lymphomahistone deacetylase inhibitor
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Hydroxamic acid-containing histone deacetylase inhibitors potentiate the antiproliferative and apoptotic effects induced by the ribonucleotide reduct…

2008

histone deacetylase inhibitors ribonucleotide reductase inhibitors cell cycle
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Cytotoxic effects of Jay Amin hydroxamic acid (JAHA), a ferrocene-based class I histone deacetylase inhibitor, on triple-negative MDA-MB231 breast ca…

2012

The histone deacetylase inhibitors (HDACis) are a class of chemically heterogeneous anticancer agents of which suberoylanilide hydroxamic acid (SAHA) is a prototypical member. SAHA derivatives may be obtained by three-dimensional manipulation of SAHA aryl cap, such as the incorporation of a ferrocene unit like that present in Jay Amin hydroxamic acid (JAHA) and homo-JAHA [ Spencer , et al. ( 2011 ) ACS Med. Chem. Lett. 2 , 358 - 362 ]. These metal-based SAHA analogues have been tested for their cytotoxic activity toward triple-negative MDA-MB231 breast cancer cells. The results obtained indicate that of the two compounds tested, only JAHA was prominently active on breast cancer cells with a…

medicine.drug_classCell SurvivalMetallocenesAntineoplastic AgentsApoptosisToxicologyHydroxamic AcidsStructure-Activity RelationshipIn vivoAnnexinmedicineTumor Cells CulturedCytotoxic T cellHumansFerrous CompoundsSettore BIO/06 - Anatomia Comparata E Citologiachemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesDose-Response Relationship DrugMolecular StructureChemistryHistone deacetylase inhibitorCell CycleGeneral MedicineIn vitroHistone Deacetylase InhibitorsBiochemistryhistone deacetylase inhibitor breast cancer autophagy apoptosis mitochondria cell cycleApoptosisCancer researchHistone deacetylaseDrug Screening Assays AntitumorReactive Oxygen Species
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