Search results for "Up-Regulation"

showing 10 items of 455 documents

Integrative genomic and proteomic analyses identify targets for Lkb1 deficient metastatic lung tumors

2010

SummaryIn mice, Lkb1 deletion and activation of KrasG12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathw…

ProteomicsCancer ResearchLung NeoplasmsMAP Kinase Kinase 2MAP Kinase Kinase 1CELLCYCLEAMP-Activated Protein Kinasesmedicine.disease_causeMice0302 clinical medicineAMP-Activated Protein Kinase KinasesCell MovementCarcinoma Non-Small-Cell LungEnzyme InhibitorsNeoplasm MetastasisPhosphorylationLymph nodePhosphoinositide-3 Kinase Inhibitors0303 health sciencesTOR Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsGenomicsCell cycleProtein-Tyrosine KinasesPenetrance3. Good healthUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structuresrc-Family KinasesOncologySIGNALING030220 oncology & carcinogenesisDrug Therapy CombinationFemaleRNA InterferenceKRASSignal TransductionMice NudeBiologyProtein Serine-Threonine KinasesArticleProto-Oncogene Proteins p21(ras)03 medical and health sciencesCell Line TumorProto-Oncogene ProteinsmedicineCell AdhesionAnimalsHumansEpithelial–mesenchymal transitionProtein Kinase Inhibitors030304 developmental biologyFocal AdhesionsGene Expression ProfilingCell BiologyXenograft Model Antitumor AssaysMice Mutant StrainsGene expression profilingFocal Adhesion Protein-Tyrosine KinasesCancer cellCell TransdifferentiationCancer researchras ProteinsCarcinogenesis
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Proteomic Profiling of Secreted Proteins for the Hematopoietic Support of Interleukin-Stimulated Human Umbilical Vein Endothelial Cells

2013

Human umbilical cord vein endothelial cells (HUVECs) secrete a number of factors that greatly impact the proliferation and differentiation of hematopoietic stem and progenitor cells (HSPCs). These factors remain largely unknown. Here, we report on the most comprehensive proteomic profiling of the HUVEC secretome and identified 827 different secreted proteins. Two hundred and thirty-one proteins were found in all conditions, whereas 369 proteins were identified only under proinflammatory conditions following IL-1β, IL-3, and IL-6 stimulation. Thirteen proteins including complement factor b (CFb) were identified only under IL-1β and IL-3 conditions and may potentially represent HSPC prolifer…

ProteomicsSpectrometry Mass Electrospray IonizationInterleukin-1betaBiomedical EngineeringComplement C5blcsh:MedicineAntigens CD34BiologyComplement factor BUmbilical veinProinflammatory cytokineHuman Umbilical Vein Endothelial CellsHumansProgenitor cellCell ProliferationTransplantationInterleukin-6lcsh:RAntibodies MonoclonalComputational BiologyInterleukinComplement System ProteinsCell BiologyFlow CytometryHematopoietic Stem CellsMolecular biologyUp-RegulationComplement systemHaematopoiesisElectrophoresis Polyacrylamide GelInterleukin-3Stem cellPeptidesCell Transplantation
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Multiple changes induced by fibroblasts on breast cancer cells.

2010

It is now widely recognised that the cross-talk between cancer and stromal cells may play a crucial role in cancer progression. However little is known about the complex underlying molecular mechanisms that occur within the tumor microenvironment. Fibroblasts are the major stromal cells with multiple roles, especially towards both the extracellular matrix and the neighbouring cell population, including neoplastic cells. Consequently, proteomic analyses would provide a wider resource for a better understanding of the potential modulating effects exerted by fibroblasts on cancer cells. In this report we describe the effects of fibroblast stimulation on the breast cancer cell line (8701-BC) pr…

ProteomicsStromal cellProteomeCellGenes mycBreast NeoplasmsCell CommunicationBiologyBiochemistryProto-Oncogene Proteins c-mycRheumatologyCell MovementCell Line TumormedicineHumansOrthopedics and Sports MedicineNeoplasm InvasivenessSettore BIO/06 - Anatomia Comparata E CitologiaFibroblastMolecular BiologyCell ProliferationTumor microenvironmentOncogeneCancerCell BiologyFibroblastsmedicine.diseaseCoculture TechniquesCell biologyUp-RegulationGene Expression Regulation NeoplasticCytoskeletal Proteinsmedicine.anatomical_structureCulture Media ConditionedSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellNeoplastic cellproteomics breast cancer cells fibroblasts invasion assay cell proliferation.FemaleStromal CellsConnective tissue research
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TLR4 Up-regulation and Reduced Foxp3 Expression in Mechanically Ventilated Smokers with Obstructive Chronic Bronchitis

2013

Background: Chronic bronchitis (CB) is a risk factor in chronic obstructive pulmonary disease (COPD) for accelerated lung function decline and increased mortality. The lung and systemic inflammatory and immunological profile of COPD patients with CB which acutely experience respiratory failure upon a disease exacerbation is unknown. Methods: In this study, we explored the expression of Foxp3 by western blot analysis, TLR4 by immunocytochemistry and the concentrations of IP-10 and IL-8 by ELISA in the mini-bronchoalveolar lavages (mini-BAL) and in the peripheral blood of patients with respiratory failure requiring intubation and mechanical ventilation. The recruited subjects were separated i…

Pulmonary and Respiratory MedicineMaleChronic bronchitismedicine.medical_specialtyPathologyNeutrophilsmedicine.medical_treatmentSettore MED/41 - AnestesiologiaGastroenterologyStatistics NonparametricLeukocyte CountPulmonary Disease Chronic ObstructiveAcute Lung InjuryToll-like receptors Foxp3 Chemokines Smokers Respiratory failureInternal medicineMedicineHumansRisk factorAgedMechanical ventilationAged 80 and overCOPDLungbusiness.industryInterleukin-8SmokingFOXP3Forkhead Transcription Factorsmedicine.diseaseRespiration Artificialrespiratory tract diseasesUp-RegulationBronchitis ChronicChemokine CXCL10Toll-Like Receptor 4medicine.anatomical_structureRespiratory failureBronchitisFemalebusinessBronchoalveolar Lavage Fluid
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Telomerase and Telomere Length in Pulmonary Fibrosis

2013

In addition to its expression in stem cells and many cancers, telomerase activity is transiently induced in murine bleomycin (BLM)-induced pulmonary fibrosis with increased levels of telomerase transcriptase (TERT) expression, which is essential for fibrosis. To extend these observations to human chronic fibrotic lung disease, we investigated the expression of telomerase activity in lung fibroblasts from patients with interstitial lung diseases (ILDs), including idiopathic pulmonary fibrosis (IPF). The results showed that telomerase activity was induced in more than 66% of IPF lung fibroblast samples, in comparison with less than 29% from control samples, some of which were obtained from lu…

Pulmonary and Respiratory MedicineMaleTelomerasePathologymedicine.medical_specialtyClinical BiochemistryBiologyBleomycinGene Expression Regulation EnzymologicHistonesTelomerase RNA componentIdiopathic pulmonary fibrosischemistry.chemical_compoundBleomycinMiceFibrosisPulmonary fibrosismedicineAnimalsHumansEmfisema pulmonarPromoter Regions GeneticMolecular BiologyLungTelomeraseCells CulturedMice KnockoutLungAntibiotics AntineoplasticAcetylationCell BiologyArticlesFibroblastsTelomererespiratory systemmedicine.diseaseIdiopathic Pulmonary FibrosisTelomereUp-Regulationrespiratory tract diseasesmedicine.anatomical_structurechemistryPulmonsChronic DiseaseCancer researchFemaleAlveolitis Extrinsic AllergicPulmons Malalties
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Aclidinium inhibits human lung fibroblast to myofibroblast transition

2011

Background Fibroblast to myofibroblast transition is believed to contribute to airway remodelling in lung diseases such as asthma and chronic obstructive pulmonary disease. This study examines the role of aclidinium, a new long-acting muscarinic antagonist, on human fibroblast to myofibroblast transition. Methods Human bronchial fibroblasts were stimulated with carbachol (10 −8 to 10 −5  M) or transforming growth factor-β1 (TGF-β1; 2 ng/ml) in the presence or absence of aclidinium (10 −9 to 10 −7  M) or different drug modulators for 48 h. Characterisation of myofibroblasts was performed by analysis of collagen type I and α-smooth muscle actin (α-SMA) mRNA and protein expression as well as α…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyCarbacholChronic Obstructive Pulmonary DiseaseBronchiMuscarinic AntagonistsBiologyCholinergic AgonistsCollagen Type ITransforming Growth Factor beta1Downregulation and upregulationWestern blotanticholinergicCell MovementInternal medicinemedicineCOPDHumans1506RNA MessengerAutocrine signallingFibroblastMyofibroblastsCells CulturedCell Proliferationmedicine.diagnostic_testDose-Response Relationship Drugairway epitheliumCell Differentiationasthmainterstitial fibrosisFibroblastsAdenosineMolecular biologymyofibroblastActinsUp-RegulationEndocrinologymedicine.anatomical_structurePhosphorylationFibroblastCarbacholMyofibroblastmedicine.drugTropanesThorax
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Critical role of fractalkine (CX3CL1) in cigarette smoke-induced mononuclear cell adhesion to the arterial endothelium.

2012

Background Cigarette smoking is an important risk factor for the development of cardiovascular disease, yet the pathways through which this may operate are poorly understood. Therefore, the mechanism underlying cigarette smoke (CS)-induced arterial endothelial dysfunction and the potential link with fractalkine/CX3CL1 upregulation were investigated. Methods and results Stimulation of human arterial umbilical endothelial cells (HUAECs) with pathophysiological concentrations of CS extract (1% CSE) increased CX3CL1 expression. Neutralisation of CX3CL1 activity under dynamic flow conditions significantly inhibited CSE-induced mononuclear cell adhesion to HUAECs (67%). The use of small interferi…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyEndotheliumPeripheral blood mononuclear cellMiceInternal medicineCX3CR1Cell AdhesionMedicineAnimalsHumansEndothelial dysfunctionRNA Small InterferingCell adhesionNADPH oxidasebiologybusiness.industryChemokine CX3CL1MicrocirculationSmokingNOX4Membrane ProteinsNADPH Oxidasesmedicine.diseaseUp-RegulationEndothelial stem cellmedicine.anatomical_structureEndocrinologyNADPH Oxidase 5Immunologybiology.proteinEndothelium VascularbusinessThorax
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Clostridium difficile toxin A induces expression of the stress-induced early gene product RhoB.

2004

Clostridium difficile toxin A monoglucosylates the Rho family GTPases Rho, Rac, and Cdc42. Glucosylation leads to the functional inactivation of Rho GTPases and causes disruption of the actin cytoskeleton. A cDNA microarray revealed the immediate early gene rhoB as the gene that was predominantly up-regulated in colonic CaCo-2 cells after treatment with toxin A. This toxin A effect was also detectable in epithelial cells such as HT29 and Madin-Darby canine kidney cells, as well as NIH 3T3 fibroblasts. The expression of RhoB was time-dependent and correlated with the morphological changes of cells. The up-regulation of RhoB was approximately 15-fold and was based on the de novo synthesis of …

RHOAPyridinesRHOBBacterial ToxinsClostridium difficile toxin ARAC1GTPaseBiochemistryp38 Mitogen-Activated Protein KinasesGene Expression Regulation EnzymologicGene productEnterotoxinsStress PhysiologicalRhoB GTP-Binding ProteinHumansrhoB GTP-Binding ProteinMolecular BiologyOligonucleotide Array Sequence AnalysisbiologyImidazolesCell BiologyRhoBClostridium difficileActin cytoskeletonMolecular biologyUp-Regulationbiology.proteinGene expressionCaco-2 CellsThe Journal of biological chemistry
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EBV-Induced Gene 3 Transcription Is Induced by TLR Signaling in Primary Dendritic Cells via NF-κB Activation

2005

Abstract The EBV-induced gene 3 (EBI3) is expressed in dendritic cells (DCs) and part of the cytokine IL-27 that controls Th cell development. However, its regulated expression in DCs is poorly understood. In the present study we demonstrate that EBI3 is expressed in splenic CD8−, CD8+, and plasmacytoid DC subsets and is induced upon TLR signaling. Cloning and functional analysis of the EBI3 promoter using in vivo footprinting and mutagenesis showed that stimulation via TLR2, TLR4, and TLR9 transactivated the promoter in primary DCs via NF-κB and Ets binding sites at −90 and −73 bp upstream of the transcriptional start site, respectively. Furthermore, we observed that NF-κB p50/p65 and PU.1…

RNA Capsmedicine.medical_treatmentDNA Mutational AnalysisMolecular Sequence DataImmunologyAntigen-Presenting CellsReceptors Cell SurfaceBiologyCell LineMinor Histocompatibility AntigensJurkat CellsMiceCell Line TumorGene expressionmedicineAnimalsHumansImmunology and AllergyReceptors CytokinePromoter Regions GeneticGlycoproteinsMice KnockoutMembrane GlycoproteinsInnate immune systemBase SequenceToll-Like ReceptorsHEK 293 cellsNF-kappa BTLR9hemic and immune systemsEBI3Dendritic CellsMolecular biologyToll-Like Receptor 2Up-RegulationMice Inbred C57BLToll-Like Receptor 4Protein SubunitsTLR2CytokineGene Expression RegulationToll-Like Receptor 9NIH 3T3 CellsTLR4Protein BindingSignal TransductionThe Journal of Immunology
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Endothelial cells and normal breast epithelial cells enhance invasion of breast carcinoma cells by CXCR-4-dependent up-regulation of urokinase-type p…

2008

Here we show the increase of invasion of three breast cancer cell lines (8701-BC, MDA-MB-231 and SKBR3) upon long-term co-incubation with culture medium of normal microvascular endothelial cells (MVEC) and normal breast epithelial cells (HB2). The enhancement of invasion relied on the interaction of microvascular endothelial cell and normal breast epithelial cell CXCL12 (SDF1) chemokine, whose expression by breast cancer cells was very low, with the cognate CXCR4 receptor of malignant cells, which resulted in over-expression of the urokinase-type plasminogen activator receptor (uPAR) on their surfaces. uPAR over-expression, showed by RT-PCR and Western blotting, was paralleled by increased …

Receptors CXCR4MAP Kinase Kinase 4AngiogenesisCellBreast NeoplasmsReceptors Cell SurfaceCell CommunicationBiologyCell LineReceptors Urokinase Plasminogen ActivatorPathology and Forensic MedicineMetastasisangiogenesisbreast cancerTumor Cells CulturedmedicineHumansNeoplasm InvasivenessBreastSettore BIO/06 - Anatomia Comparata E CitologiaPhosphorylationskin and connective tissue diseasesCXCR4Settore MED/04 - Patologia GeneraleNeovascularization PathologicReverse Transcriptase Polymerase Chain ReactionFibrinolysisEpithelial CellsCXCL12invasionmedicine.diseasemicroenvironmentChemokine CXCL12Neoplasm ProteinsUp-RegulationEndothelial stem cellUrokinase receptormedicine.anatomical_structureCulture Media ConditionedCancer cellCancer researchFemaleJNKEndothelium VascularBreast diseaseSDF1uPARPlasminogen activatorThe Journal of Pathology
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