Search results for " c-myc"

showing 10 items of 51 documents

Differential regulation of the clusterin gene by Ha-ras and c-myc oncogenes and during apoptosis

1998

Clusterin (ApoJ) is an extracellular glycoprotein expressed during processes of tissue differentiation and regression that involve programmed cell death (apoptosis). Increased clusterin expression has also been found in tumors, however, the mechanism underlying this induction is not known. Apoptotic processes in tumors could be responsible for clusterin gene activation. Alternatively, oncogenic mutations could modulate signal transduction, thereby inducing the gene. We examined the response of the rat clusterin gene to two oncogenes, Ha-ras and c-myc, in transfected Rat1 fibroblasts. While c-myc overexpression did not modify clusterin gene activity, the Ha-ras oncogene produced a seven to t…

Cell signalingProgrammed cell deathUltraviolet RaysPhysiologyRecombinant Fusion ProteinsClinical BiochemistryGenes mycApoptosisDNA FragmentationBiologyTransfectionProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)AnimalsRNA MessengerCell Line TransformedGlycoproteinsOncogeneClusterinCell CycleCell BiologyTransfectionFibroblastsCell cycleeye diseasesRatsClusterinGenes rasApoptosisMutationCancer researchbiology.proteinsense organsSignal transductionMolecular ChaperonesSignal TransductionJournal of Cellular Physiology
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TFIIH Operates through an Expanded Proximal Promoter To Fine-Tune c-myc Expression

2004

A continuous stream of activating and repressing signals is processed by the transcription complex paused at the promoter of the c-myc proto-oncogene. The general transcription factor IIH (TFIIH) is held at promoters prior to promoter escape and so is well situated to channel the input of activators and repressors to modulate c-myc expression. We have compared cells expressing only a mutated p89 (xeroderma pigmentosum complementation group B [XPB]), the largest TFIIH subunit, with the same cells functionally complemented with the wild-type protein (XPB/wt-p89). Here, we show structural, compositional, and functional differences in transcription complexes between XPB and XPB/wt-89 cells at t…

Chromatin ImmunoprecipitationDNA ComplementaryCell SurvivalUltraviolet RaysBlotting WesternGreen Fluorescent ProteinsGene ExpressionRepressorCellular homeostasisBiologyTransfectionModels BiologicalProto-Oncogene MasProto-Oncogene Proteins c-mycTranscription Factors TFIIRibonucleasesPotassium PermanganateTranscription (biology)HumansRNA MessengerPromoter Regions GeneticMolecular BiologyModels GeneticGeneral transcription factorCell CycleGenetic Complementation TestDNA HelicasesPromoterCell BiologyFibroblastsFlow CytometryMolecular biologyDNA-Binding ProteinsKineticsTranscription Factor TFIIHMicroscopy FluorescenceMutationTranscription preinitiation complexTranscription factor II HTranscription Factor TFIIHPlasmidsMolecular and Cellular Biology
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ENO1 gene product binds to the c-myc promoter and acts as a transcriptional repressor: relationship with Myc promoter-binding protein 1 (MBP-1).

2000

The Myc promoter-binding protein-1 (MBP-1) is a 37-38 kDa protein that binds to the c-myc P2 promoter and negatively regulates transcription of the protooncogene. MBP-1 cDNA shares 97% similarity with the cDNA encoding the glycolytic enzyme alpha-enolase and both genes have been mapped to the same region of human chromosome 1, suggesting the hypothesis that the two proteins might be encoded by the same gene. We show here data indicating that a 37 kDa protein is alternatively translated from the full-length alpha-enolase mRNA. This shorter form of alpha-enolase is able to bind the MBP-1 consensus sequence and to downregulate expression of a luciferase reporter gene under the control of the c…

CytoplasmTranscriptional repressionRecombinant Fusion ProteinsBiophysicsEnolaseCodon InitiatorDown-RegulationBiologyAlternative translationResponse ElementsTransfectionBiochemistryCell LineGene productHSPA4Proto-Oncogene Proteins c-mycStructural BiologyHSPA2GeneticsBiomarkers TumorE2F1AnimalsHumansSOCS6Genes Tumor SuppressorDNA bindingPromoter Regions GeneticMolecular BiologyYY1Tumor Suppressor ProteinsNuclear ProteinsCell BiologyDNAMolecular biologyGPS2Neoplasm ProteinsDNA-Binding ProteinsMolecular WeightRepressor ProteinsAlternative SplicingGATAD2BChromosomes Human Pair 1Phosphopyruvate HydrataseProtein BiosynthesisPeptidesProtein BindingFEBS letters
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SELECTIVE G-QUADRUPLEX STABILIZERS: SALPHEN-LIKE COMPLEXES WITH ANTIPROLIFERATIVE ACTIVITY

2013

Schiff base complexes derived from N,N!-bridged tetradentate ligands involving N2O2 donor atoms present very favourable features to act as G4 binders. Thus, a series of square-planar and square pyramidal metal complexes, ML2+ (M = Ni, Cu, and Zn), have been synthesized and characterized.

G-QUADRUPLEX STABILIZERS Schiff base complexes hTelo and c-myc G-quadruplexes DNASettore CHIM/03 - Chimica Generale E InorganicaSettore BIO/10 - BiochimicaSettore CHIM/08 - Chimica Farmaceutica
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Inhibition of the HER2 pathway by n-3 polyunsaturated fatty acids prevents breast cancer in fat-1 transgenic mice

2013

Overexpression of the tyrosine kinase receptor, ErbB2/HER2/Neu, occurs in 25–30% of invasive breast cancer (BC) with poor patient prognosis. Due to confounding factors, inconsistencies still remain regarding the protective effects of n-3 polyunsaturated fatty acids (PUFAs) on BC. We therefore evaluated whether fat-1 transgenic mice, endogenously synthesizing n-3 PUFAs from n-6 PUFAs, were protected against BC development, and we then aimed to study in vivo a mechanism potentially involved in such protection. E0771 BC cells were implanted into fat-1 and wild-type (WT) mice. After tumorigenesis examination, we analyzed the expression of proteins involved in the HER2 signaling pathway and lipi…

Genetically modified mouseFatty Acid DesaturasesDocosahexaenoic AcidsReceptor ErbB-3Receptor ErbB-2Breast NeoplasmsMice TransgenicQD415-436Biologymedicine.disease_causexenograft preventionBiochemistryReceptor tyrosine kinaseProto-Oncogene Proteins c-mycMiceEndocrinologyDownregulation and upregulationCell Line TumorFatty Acids Omega-3medicineAnimalsHumansCaenorhabditis elegans ProteinsResearch ArticlesCell Proliferationchemistry.chemical_classificationCell growthCell BiologyXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticMice Inbred C57BLchemistryDocosahexaenoic acidImmunologyn-3 tissue enrichmentbiology.proteinCancer researchFemaleSignal transductionCarcinogenesispolyunsaturated fatty acid-derived mediatorsPolyunsaturated fatty acidSignal TransductionJournal of Lipid Research
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Drp1 Controls Effective T Cell Immune-Surveillance by Regulating T Cell Migration, Proliferation, and cMyc-Dependent Metabolic Reprogramming

2018

Summary Mitochondria are key players in the regulation of T cell biology by dynamically responding to cell needs, but how these dynamics integrate in T cells is still poorly understood. We show here that the mitochondrial pro-fission protein Drp1 fosters migration and expansion of developing thymocytes both in vitro and in vivo. In addition, we find that Drp1 sustains in vitro clonal expansion and cMyc-dependent metabolic reprogramming upon activation, also regulating effector T cell numbers in vivo. Migration and extravasation defects are also exhibited in Drp1-deficient mature T cells, unveiling its crucial role in controlling both T cell recirculation in secondary lymphoid organs and acc…

Genetics and Molecular Biology (all)0301 basic medicinecell migrationT-LymphocytesCellCell CountMitochondrionLymphocyte ActivationBiochemistryCell MovementHomeostasismetabolic reprogrammingcell migration; cell proliferation; cMyc; Drp1; exhaustion; metabolic reprogramming; mitochondrial dynamics; T cells; thymocytes; tumor immune-surveillance; Biochemistry Genetics and Molecular Biology (all)lcsh:QH301-705.5cMycImmunologic SurveillanceMice KnockoutThymocytesEffectorDrp1; T cells; cMyc; cell migration; cell proliferation; exhaustion; metabolic reprogramming; mitochondrial dynamics; thymocytes; tumor immune-surveillanceCell migrationCell DifferentiationCell biologymedicine.anatomical_structurePhenotypeDynaminsendocrine systemSettore BIO/06Cell SurvivalLymphoid TissueMAP Kinase Signaling SystemT cellT cellsReceptors Antigen T-CellDrp1BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleProto-Oncogene Proteins c-myc03 medical and health sciencestumor immune-surveillancemitochondrial dynamicexhaustionHomeostasimedicineAnimalsCell ProliferationTumor microenvironmentBiochemistry Genetics and Molecular Biology (all)Cell growthAnimalT cellthymocytemitochondrial dynamicsDynamin030104 developmental biologylcsh:Biology (General)T-LymphocyteT cell migration
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Two distinct amplification events of the c-myc locus in a colorectal tumour.

2008

Southern hybridisation of genomic DNA extracted from a human primary colorectal carcinoma revealed amplification of a fragment containing the wild-type c-myc locus. Two additional rearranged DNA fragments, lying upstream of c-myc, fused to distant non-contiguous sequences from the same chromosome, with an opposite configuration (head to head vs. head to tail), were also found to be amplified. Sequences analysis suggested that these rearrangements resulted from illegitimate recombination at two distinct points within the DNA sequence just upstream of the c-myc ORF and further that these events triggered two different amplification mechanisms, only one of which, involving a strand invasion ev…

GeneticsBase SequencePhysiologyMolecular Sequence DataClinical BiochemistryGene AmplificationGenes mycColorectal tumourLocus (genetics)Cell BiologyBiologyMolecular biologyDNA sequencingBlotting Southernchemistry.chemical_compoundgenomic DNAchemistryGene duplicationHumansStrand invasionColorectal Neoplasmsgene amplification c-myc CRCDNARecombination
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Apoptosis and cell growth arrest in A375 human melanoma cells by diorganotin(IV) and triorganotin(IV) complexes of [meso-Tetra(4-sulfonatophenyl)porp…

2011

In previous studies we have demonstrated that two derivatives of meso-Tetra(4-sulfonatophenyl)porphine (TPPS), (Bu2Sn)2TPPS and (Bu3Sn)4TPPS, cause apoptotic death of A375 melanoma cells and, at lower concentrations, arrest of cell proliferation. In the present study, we examined if the manganese metal inside the porphyrin cavity could improve the efficacy of this class of compounds. Thus, [meso- Tetra(4-sulfonatophenyl)porphine]Mn(III)Cl (=MnTPPS) derivatives, namely (Me2Sn)2MnTPPS, (Bu2Sn)2MnTPPS, (Me3Sn)4MnTPPS and (Bu3Sn)4MnTPPS, were tested on the A375 human melanoma cell line. A cytotoxicity assay showed that (Bu2Sn)2MnTPPS and (Bu3Sn)4MnTPPS were highly cytotoxic by inducing apoptosi…

HoechstCancer ResearchPorphyrinsSkin NeoplasmsMetalloporphyrinsDrug Evaluation PreclinicalAntineoplastic AgentsApoptosisDNA Fragmentationß-cateninBiology010402 general chemistry01 natural sciencesChloridesc-mycCell Line TumorsnailOrganotin CompoundsHumansCytotoxic T cellViability assayCytotoxicityMelanomacell viabilityCell Proliferation010405 organic chemistryCell growthCell cycleMolecular biology0104 chemical sciences3. Good healthManganese CompoundsOncologyCell cultureApoptosisDNA fragmentationcell viability; ß-catenin; c-myc; snail; HoechstInternational Journal of Oncology
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MYC Activates Stem-like Cell Potential in Hepatocarcinoma by a p53-Dependent Mechanism

2014

Activation of c-MYC is an oncogenic hallmark of many cancers including liver cancer, and is associated with a variety of adverse prognostic characteristics. Despite a causative role during malignant transformation and progression in hepatocarcinogenesis, consequences of c-MYC activation for the biology of hepatic cancer stem cells (CSCs) are undefined. Here, distinct levels of c-MYC over-expression were established by using two dose-dependent tetracycline inducible systems in 4 hepatoma cell lines with different p53 mutational status. The CSCs were evaluated using side-population approach as well as standard in vitro and in vivo assays. Functional repression of p53 was achieved by lentivira…

Homeobox protein NANOGCancer ResearchCarcinoma HepatocellularCarcinogenesisMice SCIDBiologymedicine.disease_causeArticleMalignant transformationProto-Oncogene Proteins c-mycSide populationMice Inbred NODCancer stem cellmedicineAnimalsHumansLiver NeoplasmsHep G2 Cellsmedicine.diseaseTumor BurdenTransplantationPhenotypeOncologyImmunologyNeoplastic Stem CellsCancer researchTumor Suppressor Protein p53Liver cancerCarcinogenesisReprogrammingNeoplasm TransplantationCancer Research
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Arylpyridines, arylpyrimidines and related compounds as potential modulator agents of the VEGF, hTERT and c-Myc oncogenes.

2019

Twenty-four derivatives structurally related to honokiol have been synthesized and biologically evaluated. IC50 values were determined towards the HT-29, MCF-7 and HEK-293 cell lines. Some of these derivatives exhibited comparable or lower IC50 values than honokiol towards the HT-29 and MCF-7 cell lines or else higher selectivity indexes than the natural product. Twelve selected derivatives were evaluated for their ability to inhibit the expression of the VEGFA, hTERT and c-Myc genes and also to inhibit the production of total c-Myc protein and the secretion of the VEGF protein. One of the most promising compounds, 3-(2,4-dimethoxyphenyl)pyridine, may be a good candidate for further studies…

Honokiolantiproliferative activityVascular Endothelial Growth Factor APyridinesClinical Biochemistryaza and diazabiphenyl derivativesPharmaceutical ScienceDown-RegulationGene ExpressionAntineoplastic Agents01 natural sciencesBiochemistrygene targetingProto-Oncogene Proteins c-mycchemistry.chemical_compoundanticancer agentsCell Line TumorDrug DiscoveryGene expressionHumansSecretionTelomerase reverse transcriptaseMolecular BiologyTelomeraseCell ProliferationNatural product010405 organic chemistryOrganic ChemistryGene targeting0104 chemical sciences010404 medicinal & biomolecular chemistryVascular endothelial growth factor AHEK293 CellsPyrimidineschemistryCell cultureProtein BiosynthesisCancer researchMolecular MedicineBioorganicmedicinal chemistry
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