Search results for "Oncogene Proteins"

showing 10 items of 796 documents

MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
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MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis

2017

Atherothrombotic vascular disease is often triggered by a distinct type of atherosclerotic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap that overlies the core. A key cause of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolution in atherosclerosis are incompletely understood. Here, we provide evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective…

0301 basic medicineCarotid Artery DiseasesMalePathologymedicine.medical_specialtyNecrosisCardiology030204 cardiovascular system & hematologyBiologyC-Mer Tyrosine KinaseProinflammatory cytokine03 medical and health sciencesMiceNecrosis0302 clinical medicineProto-Oncogene ProteinsmedicineAnimalsHumansEfferocytosisMice Knockoutc-Mer Tyrosine KinaseBrief ReportFibrous capReceptor Protein-Tyrosine KinasesGeneral MedicineMERTKPlaque Atherosclerotic030104 developmental biologymedicine.anatomical_structureReceptors LDLApoptosisProteolysisFemalemedicine.symptomTyrosine kinase
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Extracellular histones activate autophagy and apoptosis via mTOR signaling in human endothelial cells.

2018

Circulating histones have been proposed as targets for therapy in sepsis and hyperinflammatory symptoms. However, the proposed strategies have failed in clinical trials. Although different mechanisms for histone-related cytotoxicity are being explored, those mediated by circulating histones are not fully understood. Extracellular histones induce endothelial cell death, thereby contributing to the pathogenesis of complex diseases such as sepsis and septic shock. Therefore, the comprehension of cellular responses triggered by histones is capital to design effective therapeutic strategies. Here we report how extracellular histones induce autophagy and apoptosis in a dose-dependent manner in cu…

0301 basic medicineCell SurvivalEndothelial cellsFisiologiaApoptosisAMP-Activated Protein KinasesHistones03 medical and health sciencesExtracellularAutophagyHuman Umbilical Vein Endothelial CellsAutophagy-Related Protein-1 HomologHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologyDose-Response Relationship DrugChemistryTOR Serine-Threonine KinasesAutophagyIntracellular Signaling Peptides and ProteinsAMPKNuclear ProteinsCirculating histonesCell biologyToll-like receptorsEndothelial stem cell030104 developmental biologyHistoneApoptosisbiology.proteinMolecular MedicineProto-Oncogene Proteins c-aktSignal TransductionBiochimica et biophysica acta. Molecular basis of disease
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Chemopreventive Property of Sencha Tea Extracts towards Sensitive and Multidrug-Resistant Leukemia and Multiple Myeloma Cells

2020

The popular beverage green tea possesses chemopreventive activity against various types of tumors. However, the effects of its chemopreventive effect on hematological malignancies have not been defined. In the present study, we evaluated antitumor efficacies of a specific green tea, sencha tea, on sensitive and multidrug-resistant leukemia and a panel of nine multiple myelomas (MM) cell lines. We found that sencha extracts induced cytotoxicity in leukemic cells and MM cells to different extents, yet its effect on normal cells was limited. Furthermore, sencha extracts caused G2/M and G0/G1 phase arrest during cell cycle progression in CCRF/CEM and KMS-12-BM cells, respectively. Specifically,…

0301 basic medicineCell Survivalnatural productsgreen tealcsh:QR1-502Cell morphologychemotherapyBiochemistryArticlelcsh:Microbiologyfunctional foodPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCell Line TumorHumansCytotoxicityMolecular BiologyProtein kinase BcatechinsPI3K/AKT/mTOR pathwaypolyphenolsCell ProliferationMembrane Potential MitochondrialLeukemiadrug resistanceTeaPlant ExtractsChemistryCell growthCell CycleNF-kappa BCell cycleAntineoplastic Agents PhytogenicDrug Resistance MultipleGene Expression Regulation Neoplastic030104 developmental biologyDrug Resistance NeoplasmApoptosisCell culture030220 oncology & carcinogenesisflavonoidsCancer researchmicroarray analysisMultiple MyelomaReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSignal TransductionBiomolecules
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Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer.

2020

Cancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness and metastatic potential. Cancer cells adequately adapt cell metabolism and integrate several intracellular and redox signaling to promote cell survival in an inflammatory and hypoxic microenvironment in order to maintain/expand tumor phenotype. The administration of tyrosine kinase inhibitor (TKI) constitutes the recommended therapeutic strategy in different malignancies at advanced stages. There are important interrelationships between cell stress, redox status, mitochondrial function, metabolism and cellular signali…

0301 basic medicineCell deathCell signalingClinical BiochemistryPGC-1αApoptosisReview ArticleBiochemistryReceptor tyrosine kinase03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsAutophagyTumor MicroenvironmentHumansProtein kinase AProtein kinase Blcsh:QH301-705.5Protein Kinase InhibitorsPI3K/AKT/mTOR pathwaylcsh:R5-920biologyOrganic ChemistryMitochondria030104 developmental biologylcsh:Biology (General)Redox statusCancer cellbiology.proteinCancer researchEndoplasmic reticulum stressmTORSignal transductionlcsh:Medicine (General)Tyrosine kinaseProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryRedox biology
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MYC Induces a Hybrid Energetics Program Early in Cell Reprogramming

2018

Summary Cell reprogramming is thought to be associated with a full metabolic switch from an oxidative- to a glycolytic-based metabolism. However, neither the dynamics nor the factors controlling this metabolic switch are fully understood. By using cellular, biochemical, protein array, metabolomic, and respirometry analyses, we found that c-MYC establishes a robust bivalent energetics program early in cell reprogramming. Cells prone to undergo reprogramming exhibit high mitochondrial membrane potential and display a hybrid metabolism. We conclude that MYC proteins orchestrate a rewiring of somatic cell metabolism early in cell reprogramming, whereby somatic cells acquire the phenotypic plast…

0301 basic medicineCell signalingSomatic cellCèl·lulesCellOxidative phosphorylationcell reprogramming cell signaling metabolism mitochondrial dynamicsBiologyHybrid CellsBiochemistryMitochondrial DynamicsArticleOxidative PhosphorylationMitocondrisProto-Oncogene Proteins c-myc03 medical and health sciencesMetabolomicsCDC2 Protein KinaseGeneticsmedicinecell signalingAnimalsHumansGlycolysisPhosphorylationlcsh:QH301-705.5Membrane potentialMembrane Potential Mitochondriallcsh:R5-920cell reprogrammingCell BiologyCellular ReprogrammingCell biologyMitochondriaMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:Medicine (General)ReprogrammingmetabolismGlycolysisDevelopmental Biology
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MOBP levels are regulated by Fyn kinase and affect the morphological differentiation of oligodendrocytes.

2015

Oligodendrocytes are the myelinating glial cells of the central nervous system (CNS). Myelin is formed by extensive wrapping of oligodendroglial processes around axonal segments which ultimately allows a rapid saltatory conduction of action potentials within the CNS and sustains neuronal health. The non-receptor tyrosine kinase Fyn is an important signaling molecule in oligodendrocytes. It controls the morphological differentiation of oligodendrocytes and is an integrator of axon-glial signaling cascades leading to localized synthesis of Myelin Basic Protein (MBP) which is essential for myelin formation. The abundant Myelin-Associated Oligodendrocytic Basic Protein (MOBP) resembles MBP in s…

0301 basic medicineCellular differentiationCentral nervous systemGene ExpressionBiologyProto-Oncogene Proteins c-fyn03 medical and health sciencesMyelinFYNmedicineAnimalsCell ShapeCells CulturedSaltatory conductionCell DifferentiationCell BiologyOligodendrocyteMyelin basic proteinCell biologyMice Inbred C57BLOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemBiochemistryProtein Biosynthesisbiology.proteinTyrosine kinaseMyelin ProteinsJournal of cell science
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NFATc1 releases BCL6-dependent repression of CCR2 agonist expression in peritoneal macrophages fromSaccharomyces cerevisiaeinfected mice

2016

The link between the extensive usage of calcineurin (CN) inhibitors cyclosporin A and tacrolimus (FK506) in transplantation medicine and the increasing rate of opportunistic infections within this segment of patients is alarming. Currently, how peritoneal infections are favored by these drugs, which impair the activity of several signaling pathways including the Ca(++) /CN/NFAT, Ca(++) /CN/cofilin, Ca(++) /CN/BAD, and NF-κB networks, is unknown. Here, we show that Saccharomyces cerevisiae infection of peritoneal resident macrophages triggers the transient nuclear translocation of NFATc1β isoforms, resulting in a coordinated, CN-dependent induction of the Ccl2, Ccl7, and Ccl12 genes, all enc…

0301 basic medicineChemokineReceptors CCR2Calcineurin InhibitorsImmunologySaccharomyces cerevisiaeOpportunistic InfectionsCCL7MonocytesMice03 medical and health sciences0302 clinical medicineCyclosporin aAnimalsProtein IsoformsImmunology and AllergyChemokine CCL7Promoter Regions GeneticCCL12Transcription factorChemokine CCL2NFATC Transcription FactorsbiologyCalcineurinNF-kappa BNFATNFATC Transcription FactorsMonocyte Chemoattractant Proteins3. Good healthCalcineurinProtein Transport030104 developmental biology030220 oncology & carcinogenesisMacrophages PeritonealProto-Oncogene Proteins c-bcl-6biology.proteinCancer researchEuropean Journal of Immunology
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The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress

2015

The MRE11/RAD50/NBS1 (MRN) complex is a major sensor of DNA double strand breaks, whose role in controlling faithful DNA replication and preventing replication stress is also emerging. Inactivation of the MRN complex invariably leads to developmental and/or degenerative neuronal defects, the pathogenesis of which still remains poorly understood. In particular, NBS1 gene mutations are associated with microcephaly and strongly impaired cerebellar development, both in humans and in the mouse model. These phenotypes strikingly overlap those induced by inactivation of MYCN, an essential promoter of the expansion of neuronal stem and progenitor cells, suggesting that MYCN and the MRN complex migh…

0301 basic medicineDNA ReplicationTranscription GeneticDNA damageDNA repairDNA-Binding ProteinCell Cycle ProteinsBiology03 medical and health sciencesMRE11 Homologue ProteinCell Cycle ProteinStrand-Break Repair; N-Myc; Dna-Replication; Human Neuroblastoma; Feingold-Syndrome; C-Myc; Mre11-Rad50-Nbs1 Complex; Targeted Disruption; Genomic Instability; Embryonic LethalityHumansProgenitor cellMolecular BiologyneoplasmsCells CulturedNuclear ProteinCell ProliferationGeneticsNeuronsOncogene ProteinsOriginal PaperMRE11 Homologue ProteinN-Myc Proto-Oncogene ProteinCell growthDNA Repair EnzymeDNA replicationOncogene ProteinNuclear ProteinsCell BiologyNeuronCell biologyAcid Anhydride HydrolasesDNA-Binding Proteins030104 developmental biologyDNA Repair EnzymesMRN complexGene Expression RegulationRad50HumanCell Death and Differentiation
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Contribution of allelic imbalance to colorectal cancer

2018

Point mutations in cancer have been extensively studied but chromosomal gains and losses have been more challenging to interpret due to their unspecific nature. Here we examine high-resolution allelic imbalance (AI) landscape in 1699 colorectal cancers, 256 of which have been whole-genome sequenced (WGSed). The imbalances pinpoint 38 genes as plausible AI targets based on previous knowledge. Unbiased CRISPR-Cas9 knockout and activation screens identified in total 79 genes within AI peaks regulating cell growth. Genetic and functional data implicate loss of TP53 as a sufficient driver of AI. The WGS highlights an influence of copy number aberrations on the rate of detected somatic point muta…

0301 basic medicineDenmarkLoss of HeterozygosityGeneral Physics and AstronomyAllelic ImbalanceLoss of heterozygosityGenotypeddc:576.5RNA Small Interferinglcsh:ScienceRNA Small Interfering/geneticsGeneticsMultidisciplinaryQGenomicsPhenotype3. Good healthGENOMEPhenotypesyöpägeenitAllelic ImbalanceTumor Suppressor Protein p53/geneticsColorectal NeoplasmsChromosomes Human Pair 8GENESDNA Copy Number VariationsGenotypeScienceTranscription Factors/geneticsGenomicscolorectal cancerBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins p21(ras)Proto-Oncogene Proteins p21(ras)/genetics03 medical and health sciencesmedicineHumansPoint MutationGenetic Predisposition to DiseaseGenepaksusuolisyöpäChromosome AberrationsWhole Genome SequencingHUMAN-COLONGene Expression ProfilingPoint mutationCancerGeneral Chemistrymedicine.diseaseColorectal Neoplasms/geneticsENHANCERS030104 developmental biologyCELLSlcsh:Q3111 BiomedicineTumor Suppressor Protein p53CRISPR-Cas SystemsmutaatiotTranscription FactorsMicrosatellite Repeats
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