Search results for "Histone"

showing 10 items of 522 documents

Negative transcriptional control of ERBB2 gene by MBP-1 and HDAC1: diagnostic implications in breast cancer

2013

Abstract Background The human ERBB2 gene is frequently amplified in breast tumors, and its high expression is associated with poor prognosis. We previously reported a significant inverse correlation between Myc promoter-binding protein-1 (MBP-1) and ERBB2 expression in primary breast invasive ductal carcinoma (IDC). MBP-1 is a transcriptional repressor of the c-MYC gene that acts by binding to the P2 promoter; only one other direct target of MBP-1, the COX2 gene, has been identified so far. Methods To gain new insights into the functional relationship linking MBP-1 and ERBB2 in breast cancer, we have investigated the effects of MBP-1 expression on endogenous ERBB2 transcript and protein lev…

Cancer ResearchMBP-1/EnolaseReceptor ErbB-2Breast NeoplasmsHistone Deacetylase 1BiologyERBB geneBreast cancerTranscriptional regulationTranscription (biology)Histone DeacetylaseBreast CancermedicineTranscriptional regulationBiomarkers TumorTumor Cells CulturedGeneticsHumansMBP-1ERBB2Promoter Regions Geneticskin and connective tissue diseasesGeneReporter geneCarcinoma Ductal BreastCancerTransfectionGenes erbB-2medicine.diseaseImmunohistochemistryHDAC1Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticSettore BIO/18 - GeneticaOncologyCancer researchChromatin immunoprecipitationResearch ArticleBMC Cancer
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Oligodendroglioma cells synthesize the differentiation-specific linker histone H1˚ and release it into the extracellular environment through shed ves…

2013

Chromatin remodelling can be involved in some of the epigenetic modifications found in tumor cells. One of the mechanisms at the basis of chromatin dynamics is likely to be synthesis and incorporation of replacement histone variants, such as the H1° linker histone. Regulation of the expression of this protein can thus be critical in tumorigenesis. In developing brain, H1° expression is mainly regulated at the post-transcriptional level and RNA-binding proteins (RBPs) are involved. In the past, attention mainly focused on the whole brain or isolated neurons and little information is available on H1° expression in other brain cells. Even less is known relating to tumor glial cells. In this st…

Cancer ResearchOligodendrogliomaGene Expressionmedicine.disease_causeHistonessheddingHistone H1Settore BIO/10 - BiochimicaGene expressionmedicineAnimalsRNA MessengerEpigeneticsRats WistarSettore BIO/06 - Anatomia Comparata E CitologiaTransport Vesicleshistone variantsCells CulturedCell NucleusMessenger RNAbiologyBrain NeoplasmsastrocytesBrainRNA-Binding ProteinsArticlesH1° histoneCell cycleChromatin Assembly and DisassemblyRatsChromatinCell biologyCell Transformation Neoplasticoligodendroglioma cellsHistoneOncologyoligodendroglioma cells astrocytes post-transcriptional regulation histone variants H1˚ histone RNA-binding proteins extracellular vesicles sheddingbiology.proteinextracellular vesiclesCarcinogenesispost-transcriptional regulation
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MLL-Rearranged Leukemia Is Dependent on Aberrant H3K79 Methylation by DOT1L

2011

SummaryThe histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations of the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in an MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3, and H3K36me3 in hematopoietic progenitor and leukemia stem cells (LSCs). We found abnormal profiles only for H3K79me2 on MLL-AF9 fusion target loci in LSCs. Inactivation of Dot1l led to downregulation of direct MLL-AF9 targets and an MLL translocation-associated gene expression signature, whereas global gene expression remained largely unaffected. Suppression of MLL translocation-a…

Cancer ResearchOncogene Proteins FusionCellular differentiationApoptosisBiologyMethylationArticleHistonesMice03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineAnimalsHumansEpigeneticsMyeloid Ecotropic Viral Integration Site 1 ProteinneoplasmsMyeloid Progenitor Cells030304 developmental biologyGene RearrangementHomeodomain Proteins0303 health sciencesLysineMyelodysplastic syndromesCell CycleCell DifferentiationCell BiologyHistone-Lysine N-MethyltransferaseMethyltransferasesMethylationDOT1Lmedicine.diseaseMolecular biologyHematopoiesisNeoplasm Proteins3. Good healthLeukemiaCell Transformation NeoplasticOncologyGenetic Loci030220 oncology & carcinogenesisHistone methyltransferaseCancer researchH3K4me3Protein Processing Post-TranslationalMyeloid-Lymphoid Leukemia ProteinCancer Cell
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Histone deacetylase inhibitors induce in human hepatoma HepG2 cells acetylation of p53 and histones in correlation with apoptotic effects

2007

This report shows that histone deacetylase inhibitors (HDACIs) induced apoptosis in human hepatoma HepG2 cells in a dose- and time-dependent manner. Trichostatin A (TSA), ITF2357 and suberoylanilide hydroxamic acid (SAHA), which were very effective agents, caused apoptotic effects after a lag phase of 12-16 h. In order to elucidate the mechanism of HDACIs action in HepG2 cells we have studied the effects of TSA, ITF2357 and SAHA on acetylation of p53 and histones H2A, H2B, H3 and H4. It was observed that HDACIs rapidly induced acetylation of these proteins, being the effects clearly visible already at 30 min of treatment at the same doses which caused apoptosis. Analysis of the immunocomple…

Cancer ResearchProgrammed cell deathCarcinoma Hepatocellularmedicine.drug_classAntineoplastic AgentsApoptosisBiologyHydroxamic AcidsHistonesCell Line TumorSettore BIO/10 - BiochimicamedicineHumansBenzothiazolesEnzyme InhibitorsRNA Small InterferingHistone AcetyltransferasesVorinostatHistone deacetylase inhibitors acetylation p53 histones apoptosis hepatoma cells.Liver NeoplasmsHistone deacetylase inhibitorAcetylationProto-Oncogene Proteins c-mdm2Molecular biologyHistone Deacetylase InhibitorsTrichostatin AHistoneOncologyPCAFAcetylationbiology.proteinHistone deacetylaseTumor Suppressor Protein p53DNA DamageToluenemedicine.drugInternational Journal of Oncology
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Histone deacetylase inhibition by valproic acid down-regulates c-FLIP/CASH and sensitizes hepatoma cells towards CD95-and TRAIL receptor-mediated apo…

2005

Hepatocellular carcinoma (HCC) is highly resistant to chemotherapy, leading to a poor prognosis of advanced disease. Inhibitors of histone deacetylase (HDACi) induce re-differentiation in tumor cells and thereby re-establish sensitivity towards apoptotic stimuli. HDACi are entering the clinical stage of tumor treatment, and several substances are currently being tested in clinical trials to prove their efficacy in the treatment of leukemias and solid tumors. In this study, we investigated the impact of the HDACi valproic acid (VA) on TRAIL- and CD95-mediated apoptosis in hepatoma cells, as well as its sensitizing effect on a chemotherapeutic agent. Treatment of HepG2 cells with VA increased…

Cancer ResearchProgrammed cell deathCarcinoma Hepatocellularmedicine.medical_treatmentCellCASP8 and FADD-Like Apoptosis Regulating ProteinDown-RegulationCaspase 3ApoptosisBiologyReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansfas ReceptorEpirubicinChemotherapyMembrane GlycoproteinsCaspase 3Tumor Necrosis Factor-alphaValproic AcidLiver NeoplasmsIntracellular Signaling Peptides and ProteinsGeneral MedicineCell cycleFas receptorHistone Deacetylase Inhibitorsmedicine.anatomical_structureOncologyApoptosisDrug Resistance NeoplasmCaspasesCancer researchHistone deacetylaseApoptosis Regulatory Proteins
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Sodium phenylbutyrate induces apoptosis in human retinoblastoma Y79 cells: The effect of combined treatment with the topoisomerase I-inhibitor topote…

2001

Our results demonstrate that sodium phenylbutyrate, a compound with a low degree of toxicity, exerted a cytotoxic effect on human retinoblastoma Y79 cells in a time- and dose-dependent manner. Treatment of Y79 cells for 72 h with phenylbutyrate reduced cell viability by 63% at 2 mM and 90% at 4 mM. Cell death caused by phenylbutyrate exhibited the typical features of apoptosis, as shown by light and fluorescent microscopy. Western blot analysis demonstrated that exposure of Y79 cells to phenylbutyrate decreased the level of the antiapoptotic factor Bcl-2 and induced the activation of caspase-3, a key enzyme in the execution phase of apoptosis. Moreover, treatment with phenylbutyrate markedl…

Cancer ResearchProgrammed cell deathCell SurvivalBlotting WesternApoptosisPhenylbutyrateHistonesSettore BIO/10 - BiochimicamedicineTumor Cells CulturedHumansretinoblastoma apoptosis sodium phenylbutirateViability assayEnzyme InhibitorsbiologyCaspase 3TopoisomeraseRetinoblastomaSodium phenylbutyrateAcetylationDrug SynergismCell cyclePhenylbutyrateseye diseasesEnzyme ActivationOncologyProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinCancer researchTopotecanDrug Therapy CombinationTopoisomerase I InhibitorsTumor Suppressor Protein p53Topotecanmedicine.drug
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Resistance to diverse apoptotic triggers in multidrug resistant HL60 cells and its possible relationship to the expression of P-glycoprotein, Fas and…

2002

We studied the human HL60 leukemia cell line and its multidrug resistant (MDR) variant HL60R. In contrast to the HL60, HL60R showed an inability to undergo apoptosis from doxorubicin (Dox) or other different stimuli, including cisplatin, Fas ligation and serum withdrawal. HL60R cells lost surface Fas expression, but we found no evidence that Fas/FasL mediates the apoptotic effects of Dox in HL60. P-glycoprotein (P-gp) did not seem to play a major role as a specific inhibitor of apoptosis. In fact, the P-gp inhibitor verapamil reversed only partially the resistance to Dox-induced apoptosis of the MDR cells. In addition, it did not modify the rate of apoptosis induced from the other stimuli i…

Cancer ResearchProgrammed cell deathTime FactorsChromosomal Proteins Non-HistoneSurvivinDown-RegulationAntineoplastic AgentsApoptosisHL-60 CellsNerve Tissue ProteinsBiologyInhibitor of apoptosisFas ligandInhibitor of Apoptosis ProteinsInhibitory Concentration 50SurvivinTumor Cells CulturedHumansATP Binding Cassette Transporter Subfamily B Member 1RNA Messengerfas ReceptorP-glycoproteinInhibitor of apoptosis domainCaspase 3Reverse Transcriptase Polymerase Chain ReactionProteinsFlow CytometryNeuronal Apoptosis-Inhibitory ProteinNeoplasm ProteinsCell biologyProto-Oncogene Proteins c-bcl-2OncologyDoxorubicinDrug Resistance NeoplasmApoptosisCaspasesbiology.proteinInsect ProteinsNAIPCisplatinMicrotubule-Associated ProteinsCancer Letters
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The role of oxidative stress in apoptosis induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid in human colon adenocarcinoma …

2008

Histone deacetylase inhibitors (HDACIs) activate genes that promote cell cycle arrest and apoptosis in a number of tumor cells. This study showed that suberoylanilide hydroxamic acid (SAHA), a potent and commonly used HDACI, induced apoptosis in human colon adenocarcinoma HT-29 cells in a time- and dose-dependent manner. This effect was accompanied by the induction of oxidative stress, dissipation of mitochondrial transmembrane potential and activation of executioner caspases. Moreover, SAHA increased the levels of phosphorylated active forms of p38 and JNK. The addition of either the antioxidant N-acetylcysteine or the specific inhibitor of NADPH oxidase diphenylene iodonium chloride reduc…

Cancer ResearchProgrammed cell deathmedicine.drug_classCell Survivalp38 mitogen-activated protein kinasesBlotting WesternApoptosisAdenocarcinomamedicine.disease_causeHydroxamic AcidsAntioxidantsSettore BIO/10 - BiochimicamedicineHumansEnzyme InhibitorsProtein kinase BCaspaseMembrane Potential MitochondrialVorinostatbiologyHistone deacetylase inhibitorEnzyme ActivationHistone Deacetylase InhibitorsOxidative StressOncologyBiochemistryApoptosisCaspasesColonic NeoplasmsCancer researchbiology.proteinHistone deacetylaseReactive Oxygen Speciescolon adenomacarcinoma cells histone deacetylase inhibitors apoptosisHT29 CellsOxidative stressSignal TransductionInternational journal of oncology
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pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 multimolecular complexes mediate the transcription of estrogen receptor-…

2003

The estrogen receptor-alpha (ER) plays a crucial role in normal breast development and is also linked to development and progression of mammary carcinoma. The transcriptional repression of ER-alpha gene in breast cancer is an area of active investigation with potential clinical significance. However, the molecular mechanisms that regulate the ER-alpha gene expression are not fully understood. Here we show a new molecular mechanism of ER-alpha gene inactivation mediated by pRb2/p130 in ER-negative breast cancer cells. We investigated in vivo occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between p…

Cancer ResearchTranscription GeneticEstrogen receptorHistone Deacetylase 1HistonesTumor Cells CulturedDNA (Cytosine-5-)-MethyltransferasesReceptorPromoter Regions GeneticE2F4Nuclear ProteinsAcetylationChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticReceptors Estrogenembryonic structuresDNA methylationFemalepRb2/p130; chromatin-modifying enzymes; estrogen receptor-alpha; breast carcinomabiological phenomena cell phenomena and immunityDNA (Cytosine-5-)-Methyltransferase 1medicine.medical_specialtyanimal structuresmedicine.drug_classMacromolecular SubstancesBreast NeoplasmsE2F4 Transcription FactorBiologyHistone DeacetylasesBreast cancerInternal medicineGeneticsmedicineEstrogen Receptor betaHumansMolecular BiologyEstrogen receptor betaE2F5 Transcription FactorRetinoblastoma-Like Protein p130Estrogen Receptor alphaProteinsMethyltransferasesDNA Methylationmedicine.diseasePhosphoproteinsRepressor Proteinsenzymes and coenzymes (carbohydrates)EndocrinologyEstrogenCancer researchTrans-ActivatorsEstrogen receptor alphaTranscription FactorsOncogene
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Epigenetic Alterations Upstream and Downstream of p53 Signaling in Colorectal Carcinoma

2021

Simple Summary Colorectal cancer (CRC) belongs to the most common cancer types. It is well known that half of all CRC possess missense mutations in the TP53 tumor suppressor gene. However, the entire signaling cascade upstream and downstream of the p53 protein may also contribute to CRC development, if relevant players in this signaling cascade lost their function. Besides p53 loss-of-function by mutations, epigenetic changes (DNA methylation, post translational modifications of histones, micro-RNAs) play a vital role in CRC development. In the present review, we concentrated on the epigenetic modifications related to the entire p53 signal transduction cascade upstream and downstream of p53…

Cancer ResearchTumor suppressor genetumor suppressorUpstream and downstream (transduction)Reviewmedicine.disease_causeoncogenemicroRNAmedicineEpigeneticsneoplasmsRC254-282acetylationbiologymicro-RNANeoplasms. Tumors. Oncology. Including cancer and carcinogensMethylationdigestive system diseasesHistoneOncologyDNA methylationCancer researchbiology.proteinmethylationCarcinogenesiscarcinogenesissignal transductionCancers
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