Search results for "Autocrine signalling"

showing 10 items of 68 documents

Insulin-dependent leptin expression in breast cancer cells.

2008

Abstract Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, and diabetes, seem to increase the risk of breast cancer. Here, we studied molecular mechanisms by which insulin activates the expression of leptin, an obesity hormone that has been shown to promote breast cancer progression in an autocrine or paracrine way. Using MDA-MB-231 breast cancer cells, we found that (a) insulin stimulated leptin mRNA and protein expression, which was associated with increased activation of the leptin gene promoter; (b) insulin increased nuclear accumulation of transcription factors hypoxia inducible factor (HIF)-1α and Sp1 and their loading on the leptin promoter;…

LeptinTranscriptional ActivationCancer Researchmedicine.medical_specialtySmall interfering RNAChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternFluorescent Antibody TechniqueBreast NeoplasmsEnzyme-Linked Immunosorbent AssayBiologyParacrine signallingPhosphatidylinositol 3-Kinasesbreast cancerInternal medicinemedicineHyperinsulinemiaTumor Cells CulturedHumansHypoglycemic AgentsInsulinRNA MessengerRNA Small InterferingAutocrine signallingLuciferasesPromoter Regions GeneticTranscription factorCell NucleusMitogen-Activated Protein Kinase 1Gene knockdownLeptin receptorMitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionLeptinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaEndocrinologyOncologyCancer researchFemalehormones hormone substitutes and hormone antagonistsCancer research
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Release of IL-12 by dendritic cells activated by TLR ligation is dependent on MyD88 signaling, whereas TRIF signaling is indispensable for TLR synerg…

2010

Abstract Synergistic activation of dendritic cells by combinations of TLR ligands requires both MyD88- and TRIF-dependent signaling. Recently, it has been shown that certain combinations of TLR ligands act in synergy to induce the release of IL-12 by DCs. In this study, we sought to define the critical parameters underlying TLR synergy. Our data show that TLR ligands act synergistically if MyD88- and TRIF-dependent ligands are combined. TLR4 uses both of these adaptor molecules, thus activation via TLR4 proved to be a synergistic event on its own. TLR synergy did not affect all aspects of DC activation but enhanced primarily the release of certain cytokines, particularly IL-12, whereas the …

LipopolysaccharidesT cellImmunologyBiologyLymphocyte ActivationInterferon-gammaMicemedicineImmunology and AllergyAnimalsCD40 AntigensAutocrine signallingMice Inbred BALB CToll-Like ReceptorsSignal transducing adaptor proteinCell PolarityCell BiologyDendritic CellsInterleukin-12Cell biologyMice Inbred C57BLAdaptor Proteins Vesicular Transportmedicine.anatomical_structurePoly I-CTRIFImmunologyMyeloid Differentiation Factor 88TLR4Interleukin 12Myeloid Differentiation Factor 88Signal transductionSignal TransductionJournal of leukocyte biology
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Abstract 2484: Non-canonical Hedgehog/Gli1 signaling drives lung adenocarcinoma stem cells survival and its targeting inhibits CSC-derived tumors

2016

Abstract Introduction: Lung Adenocarcinoma (AC) is the most frequent lung cancer histological subtype and is a leading cause of cancer-related death worldwide. Hedgehog/Gli (Hh/Gli) signaling pathway regulates lung development and its aberrant activation contributes to tumor pathogenesis and play a role in cancer stem cells (CSC) control. We investigated oncogenic Hh/Gli signaling in AC-CSC. Methods: human AC-CSC were derived from primary tumors. For in vitro studies AC-CSC were maintained in serum-free medium supplemented with EGF/bFGF. For in vivo experiments, immunocompromised mice were injected with AC-CSC. Gli1 inhibitor GANT61 was used both in vitro and in vivo (IP 40 mg/kg twice/we) …

MAPK/ERK pathwayCancer Researchmedicine.medical_specialtyBiologyParacrine signallingEndocrinologyOncologyCancer stem cellGLI1Internal medicineCancer researchmedicinebiology.proteinStem cellAutocrine signallingSmoothenedHedgehogCancer Research
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Keratinocyte-Derived Granulocyte-Macrophage Colony Stimulating Factor Accelerates Wound Healing: Stimulation of Keratinocyte Proliferation, Granulati…

2001

Chronic, nonhealing wounds represent a major clinical challenge to practically all disciplines in modern medicine including dermatology, oncology, surgery, and hematology. In skin wounds, granulocyte-macrophage colony stimulating factor (GM-CSF) is secreted by keratinocytes shortly after injury and mediates epidermal cell proliferation in an autocrine manner. Many other cells involved in wound healing including macrophages, lymphocytes, fibroblasts, endothelial cells, and dendritic cells synthesize GM-CSF and/or are targets of this cytokine. Therefore, GM-CSF is a pleiotropic cytokine evoking complex processes during wound repair. Despite this complexity and the scarcity of mechanistic unde…

Macrophage colony-stimulating factorKeratinocytesMalemedicine.medical_treatmentGene ExpressionMitosisNeovascularization PhysiologicMice TransgenicDermatologytransgenic miceBiologyBiochemistryProinflammatory cytokineTransforming Growth Factor beta1MiceTransforming Growth Factor betamedicineAnimalsRNA MessengerAutocrine signallingMolecular BiologySkinWound Healingintegumentary systemGranulation tissueGranulocyte-Macrophage Colony-Stimulating FactorGM-CSFCell BiologyUp-RegulationCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyModels AnimalCancer researchCarcinogensGranulation TissueCytokinesTetradecanoylphorbol AcetateFemaleKeratinocyteWound healingmedicine.drugJournal of Investigative Dermatology
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CSF-1 signals directly to renal tubular epithelial cells to mediate repair in mice

2009

金沢大学医薬保健研究域医学系

Macrophage colony-stimulating factorPathologymedicine.medical_specialtymedicine.medical_treatmenteducation030232 urology & nephrologyApoptosisReceptor Macrophage Colony-Stimulating FactorBiology03 medical and health sciencesParacrine signallingMice0302 clinical medicineFibrosismedicineAnimalsHumansRegenerationAutocrine signalling030304 developmental biologyCell Proliferation0303 health sciencesMice Inbred C3HGrowth factorMacrophage Colony-Stimulating FactorMacrophageshemic and immune systemsEpithelial CellsGeneral Medicinemedicine.diseaseFibrosis3. Good healthKidney TubulesIntegrin alpha MApoptosisReperfusion Injurybiology.proteinCancer researchReperfusion injurytissuesResearch Article
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Colon Cancer Stem Cells Dictate Tumor Growth and Resist Cell Death by Production of Interleukin-4

2007

A novel paradigm in tumor biology suggests that cancer growth is driven by stem-like cells within a tumor. Here, we describe the identification and characterization of such cells from colon carcinomas using the stem cell marker CD133 that accounts around 2% of the cells in human colon cancer. The CD133(+) cells grow in vitro as undifferentiated tumor spheroids, and they are both necessary and sufficient to initiate tumor growth in immunodeficient mice. Xenografts resemble the original human tumor maintaining the rare subpopulation of tumorigenic CD133(+) cells. Further analysis revealed that the CD133(+) cells produce and utilize IL-4 to protect themselves from apoptosis. Consistently, trea…

MaleCD30Organoplatinum CompoundsMice NudeAntineoplastic AgentsCELLCYCLEBiologyStem cell markerMiceColon cancer interleukin-4.Cancer stem cellAntigens CDNeutralization TestsCell Line TumorSpheroids CellularGeneticsAnimalsHumansColon cancer stem cells dictate tumor growth and resist cell death by production of interleukin-4.AC133 AntigenAutocrine signallingInterleukin 4AgedGlycoproteinsLymphokine-activated killer cellCell DeathCell BiologyMiddle AgedSTEMCELLXenograft Model Antitumor AssaysCell biologyReceptors Interleukin-4OxaliplatinCell cultureembryonic structuresColonic NeoplasmsNeoplastic Stem CellsMolecular MedicineFemaleFluorouracilInterleukin-4Stem cellPeptides
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The interleukin (IL)-31/IL-31R axis contributes to tumor growth in human follicular lymphoma

2014

Interleukin (IL)-31A binds to an heterodimer composed of IL-31 receptor A (IL-31RA) and Oncostatin M Receptor (OSMR). The IL-31/IL-31R complex is involved in the pathogenesis of various skin diseases, including cutaneous T-cell lymphoma. No information is available on the relations between the IL-31/IL-31R complex and B-cell lymphoma. Here we have addressed this issue in follicular lymphoma (FL), a prototypic germinal center(GC)-derived B-cell malignancy. IL-31 enhanced primary FL cell proliferation through IL-31R-driven signal transducer and activator of transcription factor 1/3 (STAT1/3), extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt phosphorylation. In contrast, GC B cells d…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCancer ResearchPrimary Cell CultureFollicular lymphomaBiologyParacrine signallingCytosolCell-Derived MicroparticlesInternal medicinemedicineHumansProtein IsoformsPhosphorylationAutocrine signallingLymphoma FollicularCell ProliferationMitogen-Activated Protein Kinase 1B-LymphocytesMitogen-Activated Protein Kinase 3Gene Expression Regulation LeukemicInterleukinsMicrovesicleMedicine (all)Cell MembraneB-LymphocyteGerminal centerOncostatin M receptorInterleukinProtein IsoformReceptors InterleukinHematologyInterleukinMiddle Agedmedicine.diseaseGerminal CenterMolecular biologyCell-Derived MicroparticleEndocrinologySTAT1 Transcription FactorAnesthesiology and Pain MedicineOncologyFemaleSignal transductionNeoplasm GradingProto-Oncogene Proteins c-aktHumanSignal Transduction
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Extracellular Nampt promotes macrophage survival via a nonenzymatic interleukin-6/STAT3 signaling mechanism.

2008

Macrophages play key roles in obesity-associated pathophysiology, including inflammation, atherosclerosis, and cancer, and processes that affect the survival-death balance of macrophages may have an important impact on obesity-related diseases. Adipocytes and other cells secrete a protein called extracellular nicotinamide phosphoribosyltransferase (eNampt; also known as pre-B cell colony enhancing factor or visfatin), and plasma levels of eNampt increase in obesity. Herein we tested the hypothesis that eNampt could promote cell survival in macrophages subjected to endoplasmic reticulum (ER) stress, a process associated with obesity and obesity-associated diseases. We show that eNampt potent…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCell SurvivalNicotinamide phosphoribosyltransferaseApoptosisBiologyEndoplasmic ReticulumBiochemistryStat3 Signaling Pathwaychemistry.chemical_compoundParacrine signallingMicePiperidinesInternal medicinemedicineAnimalsSecretionAutocrine signallingSTAT3Nicotinamide PhosphoribosyltransferaseMolecular BiologyNicotinamide MononucleotideNicotinamide mononucleotideAcrylamidesInterleukin-6MacrophagesMechanisms of Signal TransductionCell BiologyCell biologyMice Inbred C57BLEndocrinologychemistryGene Expression Regulationbiology.proteinCytokinesSignal transductionSignal TransductionThe Journal of biological chemistry
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Natriuretic peptide system expression in murine and human submandibular salivary glands: a study of the spatial localisation of ANB, BNP, CNP and the…

2019

AbstractThe natriuretic peptide (NP) system comprises of three ligands, the Atrial Natriuretic Peptide (ANP), Brain Natriuretic peptide (BNP) and C-type Natriuretic peptide (CNP), and three natriuretic peptide receptors, NPRA, NPRB and NPRC. Here we present a comprehensive study of the natriuretic peptide system in healthy murine and human submandibular salivary glands (SMGs). We show CNP is the dominant NP in mouse and human SMG and is expressed together with NP receptors in ducts, autonomic nerves and the microvasculature of the gland, suggesting CNP autocrine signalling may take place in some of these glandular structures. These data suggest the NP system may control salivary gland funct…

MaleSettore BIO/17 - Istologia0301 basic medicinemedicine.medical_specialtyHistologyReceptors PeptidePhysiologymedicine.drug_classAtrial natriuretic peptide ANPNatriuretic peptide receptor B NPRBMice03 medical and health sciences0302 clinical medicineAtrial natriuretic peptideInternal medicineNatriuretic Peptide BrainmedicineNatriuretic peptideAnimalsHumansAutonomic nervous systemB-type natriuretic peptide BNPNatriuretic peptide receptor C NPRCAutocrine signallingReceptorSalivary glandSubmandibular glandSalivary glandC-type natriuretic peptide CNPChemistryNatriuretic Peptide C-TypeCell BiologyGeneral MedicineNatriuretic peptide receptor A NPRABrain natriuretic peptideSubmandibular glandNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureEndocrinologyOral squamous cell carcinoma030220 oncology & carcinogenesisCarcinoma Squamous CellFemaleMouth NeoplasmsAtrial Natriuretic FactorHomeostasisJournal of Molecular Histology
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The hematopoietic factor G-CSF is a neuronal ligand that counteracts programmed cell death and drives neurogenesis.

2005

G-CSF is a potent hematopoietic factor that enhances survival and drives differentiation of myeloid lineage cells, resulting in the generation of neutrophilic granulocytes. Here, we show that G-CSF passes the intact blood-brain barrier and reduces infarct volume in 2 different rat models of acute stroke. G-CSF displays strong anti-apoptotic activity in mature neurons and activates multiple cell survival pathways. Both G-CSF and its receptor are widely expressed by neurons in the CNS, and their expression is induced by ischemia, which suggests an autocrine protective signaling mechanism. Surprisingly, the G-CSF receptor was also expressed by adult neural stem cells, and G-CSF induced neurona…

Malemedicine.medical_specialtyProgrammed cell deathNeutrophilsCellular differentiationApoptosisBiologyLigandsBrain IschemiaBrain ischemiaInternal medicineGranulocyte Colony-Stimulating FactormedicineAnimalsHumansGranulocyte Precursor CellsNerve TissueRats WistarReceptorAutocrine signallingStem CellsNeurogenesisCell DifferentiationNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseNeural stem cellCell biologyRatsStrokeDisease Models AnimalEndocrinologyBlood-Brain BarrierReceptors Granulocyte Colony-Stimulating FactorStem cellResearch ArticleThe Journal of clinical investigation
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