Search results for "Histone Deacetylases"

showing 10 items of 52 documents

Class I histone deacetylases regulate p53/NF-κB crosstalk in cancer cells

2016

The transcription factors NF-κB and p53 as well as their crosstalk determine the fate of tumor cells upon therapeutic interventions. Replicative stress and cytokines promote signaling cascades that lead to the co-regulation of p53 and NF-κB. Consequently, nuclear p53/NF-κB signaling complexes activate NF-κB-dependent survival genes. The 18 histone deacetylases (HDACs) are epigenetic modulators that fall into four classes (I-IV). Inhibitors of histone deacetylases (HDACi) become increasingly appreciated as anti-cancer agents. Based on their effects on p53 and NF-κB, we addressed whether clinically relevant HDACi affect the NF-κB/p53 crosstalk. The chemotherapeutics hydroxyurea, etoposide, an…

0301 basic medicineDNA damageApoptosisModels BiologicalHistone Deacetylases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorNeoplasmsHumansHydroxyureaEpigeneticsTranscription factorCellular SenescenceEtoposidebiologyNF-kappa BNF-κBCell Cycle CheckpointsDNA NeoplasmCell BiologyHDAC6Gene Expression Regulation NeoplasticHistone Deacetylase InhibitorsCrosstalk (biology)030104 developmental biologyHistonechemistry030220 oncology & carcinogenesisMutationCancer cellbiology.proteinCancer researchTumor Suppressor Protein p53VidarabineDNA DamageSignal TransductionCellular Signalling
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Dual inhibitors of histone deacetylases and other cancer-related targets: A pharmacological perspective.

2020

International audience; Epigenetic enzymes histone deacetylases (HDACs) are clinically validated anticancer drug targets which have been studied intensively in the past few decades. Although several drugs have been approved in this field, they are still limited to a subset of hematological malignancies (in particular T-cell lymphomas), with therapeutic potential not fully realized and the drug-resistance occurred after a certain period of use. To maximize the therapeutic potential of these classes of anticancer drugs, and to extend their application to solid tumors, numerous combination therapies containing an HDACi and an anticancer agent from other mechanisms are currently ongoing in clin…

0301 basic medicineDual targeting[SDV]Life Sciences [q-bio]Cancer therapyKinasesAntineoplastic AgentsBioinformaticsBiochemistryAnticancer drugsSynergistic effectsHistone Deacetylases03 medical and health sciences0302 clinical medicineDrug Delivery SystemsNeoplasmsReceptorsmedicineAnimalsHumansEpigeneticsPharmacologybiologybusiness.industryCancerDUAL (cognitive architecture)medicine.diseaseAnticancer drug3. Good healthEnzymesClinical trial[SDV] Life Sciences [q-bio]Histone Deacetylase Inhibitors030104 developmental biologyHistone030220 oncology & carcinogenesisbiology.proteinHistone deacetylases (HDACs)EpigeneticsDual inhibitorbusinessBiochemical pharmacology
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ZNF518B gene up-regulation promotes dissemination of tumour cells and is governed by epigenetic mechanisms in colorectal cancer

2019

AbstractMost of colorectal cancer CRC-related death is due to metastasis and the finding of markers for prognosis of invasiveness, constitutes an appealing challenge. Here, after analysing cDNA array containing 43 tumour and 5 normal mucosa samples, we report that the expression of the ZNF518B gene as a whole and that of its two major splicing isoforms are significantly increased in tumours. The canonical isoform was also up-regulated in a patients’ cohort containing 70 tumour and 69 adjacent tissue samples. The effects of silencing ZNF518B on the phenotype of CRC cell lines were then studied. The gene does not affect cell proliferation, but plays a significant role in cell migration and in…

0301 basic medicineGene isoformEpithelial-Mesenchymal TransitionCelllcsh:MedicineBiologyArticleHistone DeacetylasesEpigenesis GeneticHistones03 medical and health sciences0302 clinical medicineCell MovementCell Line TumorGene expressionmedicineGene silencingHumansProtein IsoformsEpigeneticsNeoplasm Metastasislcsh:ScienceGeneCell ProliferationNeoplasm StagingMultidisciplinaryGene Expression Profilinglcsh:RPrognosisColorectal cancer3. Good healthDNA-Binding ProteinsGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structureHistoneGene Knockdown TechniquesCancer researchbiology.proteinH3K4me3lcsh:QEpigeneticsColorectal Neoplasms030217 neurology & neurosurgeryScientific Reports
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The anti-cancer drug doxorubicin induces substantial epigenetic changes in cultured cardiomyocytes.

2019

Abstract The anthracycline doxorubicin (DOX) is widely used in cancer therapy with the limitation of cardiotoxicity leading to the development of congestive heart failure. DOX-induced oxidative stress and changes of the phosphoproteome as well as epigenome were described but the exact mechanisms of the adverse long-term effects are still elusive. Here, we tested the impact of DOX treatment on cell death, oxidative stress parameters and expression profiles of proteins involved in epigenetic pathways in a cardiomyocyte cell culture model. Markers of oxidative stress, apoptosis and expression of proteins involved in epigenetic processes were assessed by immunoblotting in cultured rat myoblasts…

0301 basic medicineProgrammed cell deathMethyltransferaseApoptosisToxicologymedicine.disease_causeHistone DeacetylasesEpigenesis GeneticHistones03 medical and health sciences0302 clinical medicinemedicineAnimalsMyocytes CardiacEpigeneticsCells CulturedHistone DemethylasesAntibiotics AntineoplasticbiologyDose-Response Relationship DrugHistone deacetylase 2ChemistryGeneral MedicineEpigenomeHydrogen PeroxideCardiotoxicityCell biologyRatsOxidative Stress030104 developmental biologyHistoneAcetylationDoxorubicin030220 oncology & carcinogenesisbiology.proteinOxidative stressBiomarkersChemico-biological interactions
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Cytotoxic activity of the histone deacetylase 3-Selective inhibitor Pojamide on MDA-MB-231 triple-negative breast cancer cells

2019

We examined the effects of the ferrocene-based histone deacetylase-3 inhibitor Pojamide (N1-(2-aminophenyl)-N8-ferrocenyloctanediamide) and its two derivatives N1-(2-aminophenyl)-N6-ferrocenyladipamide and N1-(2-aminophenyl)-N8-ferroceniumoctanediamide tetrafluoroborate on triple-negative MDA-MB-231 breast cancer cells. Viability/growth assays indicated that only the first two compounds at 70 &mu

0301 basic medicineQD0901Triple Negative Breast Neoplasmslcsh:Chemistry0302 clinical medicinebreast cancer cellmitochondrial transmembrane potentialCytotoxic T cellQDSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopyTriple-negative breast cancerreactive oxygen speciesCell DeathChemistryHistone deacetylase inhibitorQapoptosisGeneral MedicineCell cycle3. Good healthComputer Science Applications030220 oncology & carcinogenesisFemalecell cycleProgrammed cell deathautophagymedicine.drug_classCell SurvivalCatalysisArticleHistone DeacetylasesInorganic Chemistry03 medical and health sciencesCell Line TumormedicineBiomarkers TumorHumansViability assayPhysical and Theoretical ChemistryMolecular Biologyhistone deacetylase inhibitorcell viabilityOrganic ChemistryAutophagyapoptosiMatrix MetalloproteinasesHistone Deacetylase InhibitorsSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999ApoptosisCancer researchQD0146breast cancer cells
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Histone deacetylase inhibition by suberoylanilide hydroxamic acid: a therapeutic approach to treat human uterine leiomyoma.

2022

Objective To evaluate the effect of inhibition of histone deacetylases (HDACs) by suberoylanilide hydroxamic acid (SAHA) treatment of human uterine leiomyoma primary (HULP) cells in vitro on cell proliferation, cell cycle, extracellular matrix (ECM) formation, and transforming growth factor β3 (TGF-β3) signaling. Design Prospective study comparing uterine leiomyoma (UL) vs. adjacent myometrium (MM) tissue and cells with or without SAHA treatment. Setting Hospital and university laboratories. Patient(s) Women with UL without any hormone treatment. Intervention(s) Myomectomy or hysterectomy surgery in women for leiomyoma disease. Main Outcome Measure(s) HDAC activity was assessed by enzyme-li…

AdultAntineoplastic AgentsHistone Deacetylase 1MMP9Histone Deacetylase 6Histone DeacetylasesCyclin D1Transforming Growth Factor beta3Cell proliferation SAHA ULS-ß3 pathway extracellular matrix uterine leiomyomaTumor Cells CulturedHumansViability assayProspective StudiesCell ProliferationVorinostatbiologyLeiomyomaChemistryCell growthCell CycleObstetrics and GynecologyCell cycleMiddle AgedHDAC3Molecular biologyProliferating cell nuclear antigenExtracellular MatrixGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsReproductive MedicineUterine Neoplasmsbiology.proteinFemaleHistone deacetylaseSignal TransductionFertility and sterility
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Histone acetylation deficits in lymphoblastoid cell lines from patients with Rubinstein-Taybi syndrome.

2012

Background: Rubinstein-Taybi syndrome (RSTS) is a congenital neurodevelopmental disorder defined by postnatal growth deficiency, characteristic skeletal abnormalities and mental retardation and caused by mutations in the genes encoding for the transcriptional co-activators with intrinsic lysine acetyltransferase (KAT) activity CBP and p300. Previous studies have shown that neuronal histone acetylation is reduced in mouse models of RSTS. Methods: The authors identified different mutations at the CREBBP locus and generated lymphoblastoid cell lines derived from nine patients with RSTS carrying distinct CREBBP mutations that illustrate different grades of the clinical severity in the spectrum …

AdultMaleAdolescentDNA Mutational AnalysisGene ExpressionHaploinsufficiencyHydroxamic AcidsHistone DeacetylasesHistonesNeurodevelopmental disorderSettore MED/38 - Pediatria Generale E SpecialisticaHistone H2AGeneticsmedicineHistone H2BHumansCREBBP geneChildGeneGenetics (clinical)Cell Line TransformedRubinstein-Taybi SyndromebiologyRubinstein–Taybi syndromeBase SequenceAcetylationmedicine.diseaseMolecular biologyCREB-Binding ProteinChromatinHistone Deacetylase InhibitorsHistoneSettore MED/03 - Genetica MedicaAcetylationChild PreschoolMutationbiology.proteinCancer researchLeukocytes MononuclearFemaleHaploinsufficiencyE1A-Associated p300 ProteinBiomarkersJournal of medical genetics
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Translocations Disrupting PHF21A in the Potocki-Shaffer-Syndrome Region Are Associated with Intellectual Disability and Craniofacial Anomalies

2012

Contains fulltext : 110038.pdf (Publisher’s version ) (Closed access) Potocki-Shaffer syndrome (PSS) is a contiguous gene disorder due to the interstitial deletion of band p11.2 of chromosome 11 and is characterized by multiple exostoses, parietal foramina, intellectual disability (ID), and craniofacial anomalies (CFAs). Despite the identification of individual genes responsible for multiple exostoses and parietal foramina in PSS, the identity of the gene(s) associated with the ID and CFA phenotypes has remained elusive. Through characterization of independent subjects with balanced translocations and supportive comparative deletion mapping of PSS subjects, we have uncovered evidence that t…

AdultMaleAdolescentGenotypePotocki–Shaffer syndromeChromosome DisordersHaploinsufficiencyBiologyHistone DeacetylasesSodium ChannelsTranslocation GeneticArticleChromatin remodelingCraniofacial Abnormalities03 medical and health sciencesSCN3A0302 clinical medicineIntellectual DisabilityNAV1.3 Voltage-Gated Sodium ChannelmedicineTranscriptional regulationGeneticsAnimalsHumansDeletion mappingGenetics(clinical)CraniofacialZebrafishGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesChromosomes Human Pair 11Infant Newbornmedicine.diseaseGenetics and epigenetic pathways of disease DCN MP - Plasticity and memory [NCMLS 6]Child PreschoolHomeoboxFemaleChromosome DeletionHaploinsufficiencyExostoses Multiple Hereditary030217 neurology & neurosurgeryThe American Journal of Human Genetics
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Use of Saccharomyces cerevisiae and Caenorhabditis elegans as model organisms to study the effect of cocoa polyphenols in the resistance to oxidative…

2011

Developing functional foods to improve the quality of life for elderly people has great economic and social impact. Searching for and validating ingredients with in vivo antioxidant effects is one of the key steps in developing this kind of food. Here we describe the combined use of simple biological models and transcriptomics to define the functional intracellular molecular targets of a polyphenol-enriched cocoa powder. Cocoa powder supplemented culture medium led to increased resistance to oxidative stress, in both the budding yeast Saccharomyces cerevisiae and the nematode Caenorhabditis elegans, and, in the latter, lifespan was also increased. These effects are fully dependent on the po…

AntioxidantSaccharomyces cerevisiae Proteinsmedicine.medical_treatmentSaccharomyces cerevisiaeGene ExpressionSaccharomyces cerevisiaemedicine.disease_causeModels BiologicalAntioxidantsHistone DeacetylasesIngredientFunctional foodPhenolsFunctional FoodmedicineAnimalsSirtuinsFood scienceCaenorhabditis elegansCaenorhabditis elegans ProteinsCaenorhabditis elegansFlavonoidsCacaobiologybusiness.industryfood and beveragesPolyphenolsForkhead Transcription FactorsGeneral Chemistrybiology.organism_classificationYeastBiotechnologyCulture MediaOxidative StressPolyphenolGeneral Agricultural and Biological SciencesbusinessOxidative stressTranscription FactorsJournal of agricultural and food chemistry
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SAHA induces apoptosis in hepatoma cells and synergistically interacts with the proteasome inhibitor Bortezomib.

2007

Histone deacetylase (HDAC) inhibitors represent a promising group of anticancer agents. This paper shows that the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) stimulated at 5-10 microM apoptosis in human hepatoma HepG2 and Huh6 cells, but was ineffective in primary human hepatocytes (PHH). In HepG2 cells SAHA induced the extrinsic apoptotic pathway, increasing the expression of both FasL and FasL receptor and causing the activation of caspase-8. Moreover, SAHA enhanced the level of Bim proteins, stimulated alternative splicing of the Bcl-X transcript with the expression of the proapoptotic Bcl-Xs isoform, induced degradation of Bid into the apoptotic factor t-Bid and dephosphorylat…

Cancer ResearchCarcinoma HepatocellularFas Ligand ProteinClinical BiochemistryPharmaceutical ScienceApoptosisHydroxamic AcidsFas ligandHistone DeacetylasesBortezomibCell Line TumormedicineHumansProtease InhibitorsProtein kinase BVorinostatHDAC inhibitors . HepG2 cells . PHH . Extrinsic and intrinsic apoptotic pathwaysbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialCaspase 8VorinostatbiologyChemistryBortezomibCytochrome cBiochemistry (medical)Cell BiologyBoronic AcidsHistone Deacetylase InhibitorsProteasomeApoptosisPyrazinesProteasome inhibitorbiology.proteinCancer researchApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
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