Search results for "PROLIFERATION"

showing 10 items of 1193 documents

Selective targeting of IRF4 by synthetic microRNA-125b-5p mimics induces anti-multiple myeloma activity in vitro and in vivo

2015

Interferon regulatory factor 4 (IRF4) is an attractive therapeutic target in multiple myeloma (MM). We here report that expression of IRF4 mRNA inversely correlates with microRNA (miR)-125b in MM patients. Moreover, we provide evidence that miR-125b is downregulated in TC2/3 molecular MM subgroups and in established cell lines. Importantly, constitutive expression of miR-125b-5p by lentiviral vectors or transfection with synthetic mimics impaired growth and survival of MM cells and overcame the protective role of bone marrow stromal cells in vitro. Apoptotic and autophagy-associated cell death were triggered in MM cells on miR-125b-5p ectopic expression. Importantly, we found that the anti-…

MaleCancer ResearchStromal cellApoptosisBiologyMiceRNA interferenceDownregulation and upregulationIn vivoIRF4Cell Line TumormicroRNAAutophagymedicineAnimalsHumansGenes Tumor SuppressorCell ProliferationmicroRNACell growthHematologyTransfectionMolecular biologymultiple myelomaMicroRNAsmedicine.anatomical_structureOncologyInterferon Regulatory FactorsCancer researchOriginal ArticleEctopic expressionBone marrow
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Promoter methylation of MGMT, MLH1 and RASSF1A tumor suppressor genes in head and neck squamous cell carcinoma: Pharmacological genome demethylation …

2012

Promoter hypermethylation of tumor suppressor genes (TSGs) is a common feature of primary cancer cells. However, to date the somatic epigenetic events that occur in head and neck squamous cell carcinoma (HNSCC) tumorigenesis have not been well-defined. In the present study, we analyzed the promoter methylation status of the genes mutL homolog 1 (MLH1), Ras-association domain family member 1 (RASSF1A) and O-6-methylguanine-DNA methyltransferase (MGMT) in 23 HNSCC samples, three control tissues and one HNSCC cell line (UM-SCC 33) using methylation-specific PCR (MSP). The expression of the three proteins was quantified by semi-quantitative immunohistochemical analysis. The cell line was treate…

MaleCancer Researchmedicine.disease_causePolymerase Chain Reactionchemistry.chemical_compoundRas association domain family member 1Genes Tumor Suppressortumor suppressor geneEnzyme InhibitorsPromoter Regions GeneticDNA Modification MethylasesAged 80 and overNuclear ProteinsArticlesGeneral MedicineMethylationMiddle AgedImmunohistochemistryPrimary tumorOncologyDealkylationHead and Neck NeoplasmsDNA methylationAzacitidineCarcinoma Squamous CellFemaleMutL Protein Homolog 1Molecular Sequence DataDown-RegulationBiologyhead and neck squamous cell carcinomamutL homolog 15-azacytidineCell Line TumormedicineHumansEpigeneticsneoplasmsO-6-methylguanine-DNA methyltransferaseAdaptor Proteins Signal TransducingAgedCell ProliferationBase SequenceDose-Response Relationship DrugTumor Suppressor ProteinsSequence Analysis DNADNA Methylationmedicine.diseaseHead and neck squamous-cell carcinomaMolecular biologyDemethylating agentSquamous carcinomastomatognathic diseasesDNA Repair EnzymeschemistryCase-Control StudiesCpG IslandsCarcinogenesisOncology Reports
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Neurogenin 3+ cells contribute to β-cell neogenesis and proliferation in injured adult mouse pancreas

2013

Abstract: We previously showed that injury by partial duct ligation (PDL) in adult mouse pancreas activates Neurogenin 3 (Ngn3)(+) progenitor cells that can differentiate to beta cells ex vivo. Here we evaluate the role of Ngn3(+) cells in beta cell expansion in situ. PDL not only induced doubling of the beta cell volume but also increased the total number of islets. beta cells proliferated without extended delay (the so-called 'refractory' period), their proliferation potential was highest in small islets, and 86% of the beta cell expansion was attributable to proliferation of pre-existing beta cells. At sufficiently high Ngn3 expression level, upto 14% of all beta cells and 40% of small i…

MaleCancer Researchmedicine.medical_specialtyendocrine systemCell- och molekylärbiologiImmunologyCellNerve Tissue Proteinsdigestive systemNeogenesisCellular and Molecular NeuroscienceMiceInternal medicineInsulin-Secreting CellsJournal ArticlemedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsInsulinRegenerationProgenitor cellBeta (finance)PancreasCell ProliferationCell SizeMice Inbred BALB CbiologydiabetesCell growthResearch Support Non-U.S. Gov'tRegeneration (biology)Cell Biologybiology.organism_classificationCell biologytissue injurycell differentiationEndocrinologymedicine.anatomical_structureOriginal ArticleHuman medicinePancreasEx vivoCell and Molecular BiologyCell Death & Disease
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Effects of peroxisome proliferator-activated receptor alpha activation on pathways contributing to cholesterol homeostasis in rat hepatocytes

2004

International audience; Peroxisome proliferator-activated receptor alpha (PPARa) activation by fibrates controls expression of several genes involved in hepatic cholesterol metabolism. Other genes could be indirectly controlled in response to changes in cellular cholesterol availability. To further understand how fibrates may affect cholesterol synthesis, we investigated in parallel the changes in the metabolic pathways contributing to cholesterol homeostasis in liver. Ciprofibrate increased HMG-CoA reductase and FPP synthase mRNA levels in rat hepatocytes, together with cholesterogenesis from [14C] acetate and [3H] mevalonate. The up-regulation observed in fenofibrate- and WY-14,643-treate…

MaleCarboxy-Lyases[SDV]Life Sciences [q-bio]Receptors Cytoplasmic and NuclearAcetatesClofibric AcidMicechemistry.chemical_compound0302 clinical medicineMice KnockoutCarbon Isotopes0303 health sciencesFenofibrateFibric AcidsPeroxisomeUp-RegulationHMG-COA REDUCTASEDNA-Binding ProteinsCholesterolCHOLESTEROL METABOLISM030220 oncology & carcinogenesisHMG-CoA reductaseCholesteryl esterPeroxisome Proliferatorslipids (amino acids peptides and proteins)Peroxisome proliferator-activated receptor alphaSterol Regulatory Element Binding Protein 1Cell DivisionSignal Transductionmedicine.drugmedicine.medical_specialtyMevalonic AcidPeroxisome ProliferationBiologyCholesterol 7 alpha-hydroxylaseBile Acids and Salts03 medical and health sciencesInternal medicinemedicineAnimalsRNA MessengerMolecular Biology030304 developmental biologyCell BiologyRAT HEPATOCYTEPPARA-NULL MOUSERatsSterol regulatory element-binding proteinMice Inbred C57BLPyrimidinesEndocrinologychemistryFIBRATECCAAT-Enhancer-Binding ProteinsHepatocytesbiology.proteinHydroxymethylglutaryl CoA ReductasesTranscription Factors
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Growth Arrest Specific 1 (Gas1) Gene Overexpression in Liver Reduces the In Vivo Progression of Murine Hepatocellular Carcinoma and Partially Restore…

2015

The prognosis of hepatocellular carcinoma patients is usually poor, the size of tumors being a limiting factor for surgical treatments. Present results suggest that the overexpression of Gas1 (growth arrest specific 1) gene reduces the size, proliferating activity and malignancy of liver tumors. Mice developing diethylnitrosamine-induced hepatocellular carcinoma were subjected to hydrodynamic gene delivery to overexpress Gas1 in liver. This treatment significantly (p < 0.05) reduced the number of large tumors, while the difference in the total number of lesions was not significant. Moreover, the number of carcinoma foci in the liver and the number of lung metastases were reduced. These resu…

MaleCarcinoma Hepatocellularlcsh:MedicineCell Cycle ProteinsGene deliveryBiologyGPI-Linked ProteinsReal-Time Polymerase Chain ReactionTransfectionMiceCell Line TumorGene expressionCarcinomamedicineAnimalslcsh:ScienceLungCell ProliferationRegulation of gene expressionMultidisciplinaryMicroarray analysis techniquesLiver Neoplasmslcsh:RCell cyclemedicine.diseaseMolecular biologyHedgehog signaling pathwayGene Expression Regulation NeoplasticLiverHepatocellular carcinomaDisease ProgressionHydrodynamicslcsh:QResearch ArticlePLoS ONE
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Chronic social stress inhibits cell proliferation in the adult medial prefrontal cortex: hemispheric asymmetry and reversal by fluoxetine treatment.

2006

Profound neuroplastic changes have been demonstrated in various limbic structures after chronic stress exposure and antidepressant treatment in animal models of mood disorders. Here, we examined in rats the effect of chronic social stress and concomitant antidepressant treatment on cell proliferation in the medial prefrontal cortex (mPFC). We also examined possible hemispheric differences. Animals were subjected to 5 weeks of daily social defeat by an aggressive conspecific and received concomitant, daily, oral fluoxetine (10 mg/kg) during the last 4 weeks. Bromodeoxyuridine (BrdU) labeling and quantitative stereological techniques were used to evaluate the treatment effects on proliferatio…

MaleCell SurvivalPrefrontal CortexCell CountFunctional Laterality03 medical and health sciences0302 clinical medicineHemispheric asymmetryFluoxetinemedicineAnimalsRats WistarPrefrontal cortexSocial Behavior030304 developmental biologyCell ProliferationPharmacologySocial stressNeurons0303 health sciencesFluoxetineDepressive DisorderCell growthStem CellsBody WeightCell DifferentiationOrgan SizeRatsPsychiatry and Mental healthBromodeoxyuridineChronic DiseaseDentate GyrusPsychologyNeuroscienceNeuroglia030217 neurology & neurosurgerySelective Serotonin Reuptake InhibitorsStress Psychologicalmedicine.drugNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
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MicroRNA signature in various cell types of mouse spermatogenesis: Evidence for stage-specifically expressed miRNA-221, -203 and -34b-5p mediated spe…

2012

Background information Recently, it became apparent that microRNAs (miRNAs) can regulate gene expression post-transcriptionally. Despite the advances in identifying the testis-expressed miRNAs and their role in spermatogenesis, only few data are available showing the spatiotemporal expression of miRNAs during this process. Results To understand how different miRNAs can regulate germ cells differentiation, we generated a transgenic mouse model and purified pure populations of premeiotic (PrM) cells and primary spermatocytes (meiotic cells). We also established spermatogonial stem cell (SSC) culture using relatively simple and robust culture conditions. Comparison of global miRNA expression i…

MaleCell typeGene ExpressionMice TransgenicBiologyCell Line03 medical and health sciencesMice0302 clinical medicinemicroRNAGene expressionTestismedicineAnimalsSpermatogenesisGeneCells Cultured030304 developmental biologyCell ProliferationGenetics0303 health sciences030219 obstetrics & reproductive medicineGene Expression ProfilingmiRNAs; spermatogenesisCell DifferentiationCell BiologyGeneral MedicineTransfectionMicroRNAsmedicine.anatomical_structureCell cultureStem cellGerm cell
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Control of Cell Migration and Inflammatory Mediators Production by CORM-2 in Osteoarthritic Synoviocytes

2011

Background Osteoarthritis (OA) is the most widespread degenerative joint disease. Inflamed synovial cells contribute to the release of inflammatory and catabolic mediators during OA leading to destruction of articular tissues. We have shown previously that CO-releasing molecules exert anti-inflammatory effects in animal models and OA chondrocytes. We have studied the ability of CORM-2 to modify the migration of human OA synoviocytes and the production of chemokines and other mediators sustaining inflammatory and catabolic processes in the OA joint. Methodology/Principal Findings OA synoviocytes were stimulated with interleukin(IL)-1β in the absence or presence of CORM-2. Migration assay was…

MaleChemokineAnatomy and PhysiologyInterleukin-1betalcsh:MedicineGene ExpressionMatrix metalloproteinaseBiochemistryCell MovementDrug Discoverylcsh:ScienceMusculoskeletal SystemCells CulturedChemokine CCL2MultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionSynovial MembraneNF-kappa BInterleukinCell migrationmedicine.anatomical_structureMedicineFemaleMatrix Metalloproteinase 3Inflammation MediatorsMatrix Metalloproteinase 1Mitogen-Activated Protein KinasesResearch ArticleCell PhysiologyBlotting WesternRheumatologySynovitisOsteoarthritisOrganometallic CompoundsmedicineHumansInterleukin 8BiologyAgedCell ProliferationChemokine CCL20lcsh:RInterleukin-8medicine.diseaseTranscription Factor AP-1CCL20Oxidative StressSmall MoleculesImmunologyCancer researchbiology.proteinlcsh:QSynovial membraneHeme Oxygenase-1PLoS ONE
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Transcription of the MAT2A gene, coding for methionine adenosyltransferase, is up-regulated by E2F and Sp1 at a chromatin level during proliferation …

2006

Methionine adenosyltransferase (MAT) is an essential enzyme because it catalyzes the formation of S-adenosylmethionine, the main methyl donor. Two MAT-encoding genes (MAT1A, MAT2A) are found in mammals. The latter is expressed in proliferating liver, dedifferentiation and cancer, whereas MAT1A is expressed in adult quiescent hepatocytes. Here, we report studies on the molecular mechanisms controlling the induction of MAT2A in regenerating rat liver and in proliferating hepatocytes. The MAT2A is up-regulated at two discrete moments during liver regeneration, as confirmed by RNApol-ChIP analysis. The first one coincides with hepatocyte priming (i.e. G0-G1 transition), while the second one tak…

MaleChromatin ImmunoprecipitationTranscription GeneticSp1 Transcription FactorMolecular Sequence DataOligonucleotidesElectrophoretic Mobility Shift AssayBiologyBiochemistryS PhaseSequence Homology Nucleic AcidmedicineAnimalsE2F1Electrophoretic mobility shift assayRats WistarPromoter Regions GeneticE2FE2F4Cells CulturedCell ProliferationSp1 transcription factorBase SequenceG1 PhaseMethionine AdenosyltransferaseCell BiologyMolecular biologyChromatinLiver regenerationE2F Transcription FactorsLiver RegenerationRatsUp-Regulationmedicine.anatomical_structureLiverMethionine AdenosyltransferaseHepatocyteHepatocytesProtein BindingThe International Journal of Biochemistry &amp; Cell Biology
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Loss of PHD3 allows tumours to overcome hypoxic growth inhibition and sustain proliferation through EGFR

2014

Solid tumours are exposed to microenvironmental factors such as hypoxia that normally inhibit cell growth. However, tumour cells are capable of counteracting these signals through mechanisms that are largely unknown. Here we show that the prolyl hydroxylase PHD3 restrains tumour growth in response to microenvironmental cues through the control of EGFR. PHD3 silencing in human gliomas or genetic deletion in a murine high-grade astrocytoma model markedly promotes tumour growth and the ability of tumours to continue growing under unfavourable conditions. The growth-suppressive function of PHD3 is independent of the established PHD3 targets HIF and NF-κB and its hydroxylase activity. Instead, l…

MaleColorectal cancerAngiogenesisProcollagen-Proline DioxygenaseGeneral Physics and AstronomyApoptosisGrowth inhibitoryBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyHypoxia-Inducible Factor-Proline DioxygenasesGene Knockout Techniqueschemistry.chemical_compoundCell Line TumormedicineAnimalsHumansEgfr signalingHypoxiaCell ProliferationMice KnockoutMultidisciplinaryCell growthGeneral ChemistryHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseMolecular biologyErbB ReceptorsOxygenchemistryApoptosisCancer researchFemalemedicine.symptomGrowth inhibitionGlioblastomaNature Communications
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