Search results for "PROLIFERATION"

showing 10 items of 1193 documents

Hsp70 is required for optimal cell proliferation in mouse A6 mesoangioblast stem cells.

2009

Mouse Hsp70 (70 kDa heat shock protein) is preferentially induced by heat or stress stimuli. We previously found that Hsp70 is constitutively expressed in A6 mouse mesoangioblast stem cells, but its possible role in these cells and the control of its basal transcription remained unexplored. Here we report that in the absence of stress, Ku factor is able to bind the HSE (heat shock element) consensus sequence in vitro, and in vivo it is bound to the proximal hsp70 promoter. In addition, we show that constitutive hsp70 transcription depends on the co-operative interaction of different factors such as Sp1 (specificity protein 1) and GAGA-binding protein with Ku factor, which binds the HSE cons…

Gene knockdownMesoangioblastBinding SitesGeneral transcription factorCell growthStem CellsCell BiologyBiologyFlow CytometryBiochemistryMolecular biologyHsp70MiceTranscription (biology)Heat shock proteinAnimalsBlood VesselsHSP70 Heat-Shock ProteinsRNA InterferenceStem cellmesoangioblast RNAi doubling timePromoter Regions GeneticMolecular BiologyCell ProliferationTranscription FactorsThe Biochemical journal
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Non-hermitian operator modelling of basic cancer cell dynamics

2018

We propose a dynamical system of tumor cells proliferation based on operatorial methods. The approach we propose is quantum-like: we use ladder and number operators to describe healthy and tumor cells birth and death, and the evolution is ruled by a non-hermitian Hamiltonian which includes, in a non reversible way, the basic biological mechanisms we consider for the system. We show that this approach is rather efficient in describing some processes of the cells. We further add some medical treatment, described by adding a suitable term in the Hamiltonian, which controls and limits the growth of tumor cells, and we propose an optimal approach to stop, and reverse, this growth.

General Physics and Astronomylcsh:AstrophysicsTumor cells01 natural sciencesArticle010305 fluids & plasmassymbols.namesakeOperatorial models; Schrödinger dynamics; non Hermitian Hamiltonian; Tumoral proliferation modelSchrödinger dynamicParticle number operatorlcsh:QB460-4660103 physical scienceslcsh:Science010306 general physicsSettore MAT/07 - Fisica MatematicaMathematical physicsPhysicsMedical treatmentOperatorial modelOther Quantitative Biology (q-bio.OT)Non hermitian HamiltonianTumoral proliferation modelQuantitative Biology - Other Quantitative Biologylcsh:QC1-999Birth–death processFOS: Biological sciencesSchrödinger dynamicsCancer cellsymbolslcsh:QOperatorial modelsHamiltonian (quantum mechanics)lcsh:PhysicsSelf-adjoint operator
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Polycystin-1 downregulation induces ERK-dependent mTOR pathway activation in a cellular model of psoriasis

2018

Psoriatic plaques tend to localize to the knees and elbows, areas that are particularly subject to mechanical stress resulting from bending and friction. Moreover, plaques often develop at sites of mechanical trauma or injury (Koebner phenomenon). Nevertheless, mechanotransduction has never been linked to psoriasis. Polycystins (polycystin-1, PC1; polycystin-2, PC2) are mechanosensitive molecules that function as key regulators of cellular mechanosensitivity and mechanotransduction. The aim of this in vitro study was to investigate the role of polycystins in the development of psoriasis. We showed that PC1 knockdown in HaCaT cells led to an elevated mRNA expression of psoriasis-related biom…

Genetic Markers0301 basic medicineMAPK/ERK pathwayendocrine systemTRPP Cation ChannelsMAP Kinase Signaling SystemDown-RegulationModels BiologicalCell Line03 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementPsoriasismedicineHumansPsoriasisMechanotransductionMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationGene knockdownCell growthChemistryTOR Serine-Threonine Kinasesmedicine.diseaseCell biologyHaCaT030104 developmental biologyGene Knockdown Techniques030220 oncology & carcinogenesisMolecular MedicineBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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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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GSK3β overexpression induces neuronal death and a depletion of the neurogenic niches in the dentate gyrus

2010

Overexpression of GSK3β in transgenic mice induces learning deficits and some features associated with Alzheimer's disease (AD), including dentate gyrus (DG) atrophy. Here, we assessed whether these mice also recapitulate DG atrophy as well as impaired neurogenesis reported in AD. Ultrastructural analysis revealed that there were fewer and more disorganized neurogenic niches in these animals, coupled with an increase in the proportion of immature neurons. Indeed, the maturation of granule cells is delayed as witnessed by the alterations to the length and patterning of their dendritic trees and to the mossy fiber terminals. Together with an increase in neuronal death, these phenomena lead to…

Genetically modified mouseProgrammed cell deathOverexpressionNeurogenesisproliferationCognitive NeuroscienceCellular differentiationeducationProliferationMice TransgenicBiologyGlycogen Synthase Kinase 3MiceAtrophyAlzheimer DiseaseMaturationmedicineAnimalsHumanshippocampal stem cellsGSK3Bhealth care economics and organizationsCell ProliferationGlycogen Synthase Kinase 3 betaCell DeathMicrogliamaturationDentate gyrusNeurogenesisGSK3 betaCell DifferentiationAlzheimer's diseasemedicine.diseaseMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureHippocampal stem cellsDentate GyrusGSK3bMicrogliaAlzheimer’s diseaseNeuroscienceoverexpressionHippocampus
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C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation

2015

Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa−/−) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa−/− mi…

Genetics and Molecular Biology (all)0301 basic medicinePROTEINGeneral Physics and AstronomyMELANOMAApoptosisInbred C57BLBiochemistryDISEASEAnimals; Apoptosis; Cell Line Tumor; Cell Movement; Cell Proliferation; Complement Activation; Complement C1q; Complement C3; Complement C5; Humans; Mice; Mice Inbred C57BL; Mice Knockout; Neoplasms; Biochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)Micefluids and secretionsCell Movementimmune system diseasesNeoplasmsIMMUNE-RESPONSEskin and connective tissue diseasesComplement ActivationComplement C1qMice KnockoutComplement component 5TumorMultidisciplinaryQChemistry (all)Complement C5Complement C33. Good healthCell biologyMultidisciplinary SciencesDEFICIENCYmedicine.anatomical_structureScience & Technology - Other TopicsHumanKnockoutSciencechemical and pharmacologic phenomenaBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyTROPHOBLAST INVASIONMECHANISMSCell LinePhysics and Astronomy (all)03 medical and health sciencesClassical complement pathwayImmune systemINFLAMMATIONCell Line TumormedicineAnimalsHumansCell ProliferationScience & TechnologyBiochemistry Genetics and Molecular Biology (all)AnimalCell growthEFFECTOR SYSTEMComplement C1qApoptosiGeneral ChemistryComplement systemMice Inbred C57BL030104 developmental biologyCancer cellNeoplasmBone marrowANTIBODY THERAPYNature Communications
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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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A BMP7 Variant Inhibits Tumor Angiogenesis In Vitro and In Vivo through Direct Modulation of Endothelial Cell Biology

2015

Bone morphogenetic proteins (BMPs), members of the TGF-β superfamily, have numerous biological activities including control of growth, differentiation, and vascular development. Using an in vitro co-culture endothelial cord formation assay, we investigated the role of a BMP7 variant (BMP7v) in VEGF, bFGF, and tumor-driven angiogenesis. BMP7v treatment led to disruption of neo-endothelial cord formation and regression of existing VEGF and bFGF cords in vitro. Using a series of tumor cell models capable of driving angiogenesis in vitro, BMP7v treatment completely blocked cord formation. Pre-treatment of endothelial cells with BMP7v significantly reduced their cord forming ability, indicating …

Genetics and Molecular Biology (all)MaleVascular Endothelial Growth Factor AFibroblast Growth FactorAngiogenesisBone Morphogenetic Protein 7Nudelcsh:MedicineSmad ProteinsFibroblast growth factorBiochemistryNeovascularizationMiceCell Movementlcsh:ScienceBMP7 Angiogenesis TumorTumorMultidisciplinaryCell DeathNeovascularization PathologicMedicine (all)Cell migrationCell biologyEndothelial stem cellSettore MED/26 - NEUROLOGIAVascular endothelial growth factor ADrug CombinationsAdipose TissueAdipose Tissue; Animals; Bone Morphogenetic Protein 7; Cell Death; Cell Line Tumor; Cell Movement; Cell Proliferation; Collagen; Drug Combinations; Endothelial Cells; Fibroblast Growth Factor 2; Glioblastoma; Human Umbilical Vein Endothelial Cells; Humans; Laminin; Male; Mice Nude; Neoplastic Stem Cells; Neovascularization Pathologic; Neovascularization Physiologic; Proteoglycans; Receptor Fibroblast Growth Factor Type 1; Signal Transduction; Smad Proteins; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Xenograft Model Antitumor Assays; Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Neoplastic Stem CellsFibroblast Growth Factor 2ProteoglycansCollagenmedicine.symptomReceptorType 1Research ArticleSignal TransductionMice NudeNeovascularization PhysiologicBMP7BiologyCell LineSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicineHuman Umbilical Vein Endothelial CellsAnimalsHumansAgricultural and Biological Sciences (all); Biochemistry Genetics and Molecular Biology (all); Medicine (all)Receptor Fibroblast Growth Factor Type 1PhysiologicNeovascularizationCell ProliferationPathologicMatrigelBiochemistry Genetics and Molecular Biology (all)lcsh:REndothelial CellsKinase insert domain receptorVascular Endothelial Growth Factor Receptor-2Xenograft Model Antitumor AssaysAgricultural and Biological Sciences (all)lcsh:QAngiogenesisLamininGlioblastomaPLoS ONE
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Mitochondrial DNA mutations in cancer--from bench to bedside.

2009

Mitochondria are cell organelles mostly known for their production of ATP through oxidative phosphorylation. As suggested over 70 years ago by O. Warburg and recently confirmed with molecular techniques, alterations in respiratory activity and mitochondrial DNA appear to be a common feature of malignant cells. Somatic mtDNA mutations have been reported in many types of cancer cells. MtDNA mutation pattern may enhance the specificity of cancer diagnostics, detection and prediction of tumor growth rate and patients' outcome. Therefore it may be used as a molecular cancer bio-marker. Nevertheless recently published papers list a large number of mitochondrial DNA mutations in many different can…

GeneticsMutationMitochondrial DNASettore BIO/16 - Anatomia UmanaSomatic cellRespiratory chainCancerContext (language use)ApoptosisMitochondrionBiologymedicine.disease_causemedicine.diseaseDNA MitochondrialModels BiologicalTranslational Research BiomedicalCell Transformation NeoplasticNeoplasmsCancer cellMutationmedicineHumansCancer Mitochondria Molecular Marker Mutation OXPHOS ReviewReactive Oxygen SpeciesCell ProliferationFrontiers in bioscience (Landmark edition)
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MAD2 depletion triggers premature cellular senescence in human primary fibroblasts by activating a P53 pathway preventing aneuploid cells propagation.

2012

The spindle assembly checkpoint (SAC) is a cellular surveillance mechanism that ensures faithful chromosome segregation during mitosis and its failure can result in aneuploidy. Previously, it was suggested that reduction of the MAD2 gene, encoding a major component of the SAC, induced aneuploidy in human tumor cells. However, tumor cell lines contain multiple mutations that might affect or exacerbate the cellular response to Mad2 depletion. Thus, the scenario resulting by Mad2 depletion in primary human cells could be different and more complex that the one depicted so far. We used primary human fibroblasts (IMR90) and epithelial breast cells (MCF10A) to gain further insight on the effects …

Genome instabilityCyclin-Dependent Kinase Inhibitor p21Cell cycle checkpointMad2PhysiologyClinical BiochemistryMAD2 depletion Aneuploidy Premature cellular senescence TP53Cell Cycle ProteinsBiologyCyclin-dependent kinaseChromosome instabilityChromosomal InstabilityTumor Suppressor Protein p14ARFHumansGene SilencingRNA Small InterferingMitosisCells CulturedCellular SenescenceCell ProliferationCalcium-Binding ProteinsCell BiologyCell Cycle CheckpointsFibroblastsAneuploidybeta-GalactosidaseCell biologyRepressor ProteinsSpindle checkpointSettore BIO/18 - GeneticaGene Expression RegulationMad2 Proteinsbiology.proteinM Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Cell agingSignal Transduction
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