Search results for "Transduction"

showing 10 items of 2149 documents

Socs3 induction by PPARγ restrains cancer-promoting inflammation

2013

The presence of proinflammatory cytokines in the tumor microenvironment can support further growth of established cancers. Docosahexaenoic acid (DHA), a peroxisome proliferator-activated receptor-gamma (PPARγ) ligand, has been shown to suppress inflammation and limit tumor progression in vivo. Are the anticancer properties of DHA relying on its ability to prevent inflammation? If so, what are the molecular links between the anti-inflammatory properties of DHA and its anticancer effects? DHA is an n-3 polyinsaturated fatty acid mainly found in fish oil that was shown to contribute to inflammation resolution by preventing the release of proinflammatory mediators in vivo.1 DHA has also been as…

STAT3 Transcription FactorDocosahexaenoic AcidsCellular differentiationPeroxisome proliferator-activated receptorInflammationSuppressor of Cytokine Signaling ProteinsBiologyEditorials: Cell Cycle FeaturesProinflammatory cytokineMicemedicineAnimalsHumansPhosphorylationPromoter Regions GeneticMolecular BiologyCells Culturedchemistry.chemical_classificationInflammationTumor microenvironmentInterleukin-17TroglitazoneCell DifferentiationCell BiologyPPAR gammaCell Transformation NeoplasticchemistryGene Expression RegulationSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer cellCancer researchTh17 CellsInterleukin 17medicine.symptomDevelopmental Biologymedicine.drugProtein BindingSignal TransductionCell Cycle
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Intracellular osteopontin protects from autoimmunity-driven lymphoma development inhibiting TLR9-MYD88-STAT3 signaling

2022

Abstract Background Autoimmune disorders, including Systemic Lupus Erythematosus (SLE), are associated with increased incidence of hematological malignancies. The matricellular protein osteopontin (OPN) has been linked to SLE pathogenesis, as SLE patients show increased serum levels of OPN and often polymorphisms in its gene. Although widely studied for its pro-tumorigenic role in different solid tumours, the role of OPN in autoimmunity-driven lymphomagenesis has not been investigated yet. Methods To test the role of OPN in the SLE-associated lymphomagenesis, the SLE-like prone Faslpr/lpr mutation was transferred onto an OPN-deficient background. Spleen from Faslpr/lpr and OPN-/-Faslpr/lpr …

STAT3 Transcription FactorMice Inbred MRL lprCancer ResearchLymphomaSettore MED/08 - Anatomia PatologicaAutoimmune DiseasesMice Inbred C57BLAutoimmunity Diffuse large B cell lymphoma OsteopontinMiceOncologyToll-Like Receptor 9Myeloid Differentiation Factor 88HumansAnimalsLupus Erythematosus SystemicSettore MED/05 - Patologia ClinicaMolecular MedicineSignal TransductionAdaptor Proteins Signal TransducingMolecular Cancer
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Tumor-Derived Small Extracellular Vesicles Induce Pro-Inflammatory Cytokine Expression and PD-L1 Regulation in M0 Macrophages via IL-6/STAT3 and TLR4…

2021

Tumor-associated macrophages play a key role in promoting tumor progression by exerting an immunosuppressive phenotype associated with the expression of programmed cell death ligand 1 (PD-L1). It is well known that tumor-derived small extracellular vesicles (SEVs) affect the tumor microenvironment, influencing TAM behavior. The present study aimed to examine the effect of SEVs derived from colon cancer and multiple myeloma cells on macrophage functions. Non-polarized macrophages (M0) differentiated from THP-1 cells were co-cultured with SEVs derived from a colorectal cancer (CRC) cell line, SW480, and a multiple myeloma (MM) cell line, MM1.S. The expression of PD-L1, interleukin-6 (IL-6), a…

STAT3 Transcription FactorPD-L1QH301-705.5colorectal cancersmall extracellular vesiclesB7-H1 AntigenArticleCatalysisStat3 Signaling PathwayProinflammatory cytokineM0 macrophageInorganic ChemistryExtracellular VesiclesSettore BIO/13 - Biologia ApplicataCell Line TumorPD-L1Tumor-Associated Macrophagessmall extracellular vesicleHumansMacrophageTLR4Biology (General)Physical and Theoretical ChemistryM0 macrophagesQD1-999Molecular BiologySpectroscopyInflammationTumor microenvironmentbiologyInterleukin-6ChemistryOrganic ChemistryGeneral MedicineComputer Science ApplicationsGene Expression Regulation NeoplasticToll-Like Receptor 4multiple myelomaChemistryCell cultureTumor progressionColonic Neoplasmsbiology.proteinCancer researchTLR4Signal TransductionInternational Journal of Molecular Sciences
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Nitric Oxide-Releasing Drug Glyceryl Trinitrate Targets JAK2/STAT3 Signaling, Migration and Invasion of Triple-Negative Breast Cancer Cells

2021

Triple-negative breast cancer (TNBC) is a highly aggressive disease with invasive and metastasizing properties associated with a poor prognosis. The STAT3 signaling pathway has shown a pivotal role in cancer cell migration, invasion, metastasis and drug resistance of TNBC cells. IL-6 is a main upstream activator of the JAK2/STAT3 pathway. In the present study we examined the impact of the NO-donor glyceryl trinitrate (GTN) on the activation of the JAK2/STAT3 signaling pathway and subsequent migration, invasion and metastasis ability of TNBC cells through in vitro and in vivo experiments. We used a subtoxic dose of carboplatin and/or recombinant IL-6 to activate the JAK2/STAT3 signaling path…

STAT3 Transcription FactorQH301-705.5Triple Negative Breast NeoplasmsmigrationArticleCatalysisStat3 Signaling PathwayMetastasisInorganic ChemistryMiceNitroglycerinchemistry.chemical_compoundCell Movementnitric oxideIn vivoCell Line TumormedicineAnimalsHumanscancermetastasisNeoplasm InvasivenessNitric Oxide DonorsBiology (General)Physical and Theoretical ChemistrySTAT3QD1-999Molecular BiologySpectroscopyTriple-negative breast cancerMice Inbred BALB CbiologyActivator (genetics)Organic ChemistryCancerGeneral MedicineJanus Kinase 2invasionmedicine.diseaseCarboplatinComputer Science ApplicationsChemistrychemistrybiology.proteinCancer researchFemalesignalingSignal TransductionInternational Journal of Molecular Sciences
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Inhibition of VEGF expression through blockade of Hif1a and STAT3 signalling mediates the anti-angiogenic effect of melatonin in HepG2 liver cancer c…

2013

Background: Hepatocellular carcinoma (HCC) growth relies on angiogenesis via vascular endothelial growth factor (VEGF) release. Hypoxia within tumour environment leads to intracellular stabilisation of hypoxia inducible factor 1 alpha (Hif1α) and signal transducer and activator of transcription (STAT3). Melatonin induces apoptosis in HCC, and shows anti-angiogenic features in several tumours. In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate the anti-angiogenic effects of melatonin. Methods: HepG2 cells were treated with melatonin under normoxic or CoCl2-induced hypoxia. Gene expression was analysed by RT–qPCR and western blot. Melatonin-induced anti-…

STAT3 Transcription FactorTranscriptional ActivationVascular Endothelial Growth Factor ACancer ResearchCarcinoma HepatocellularTranscription GeneticAngiogenesisAngiogenesis InhibitorsApoptosismelatoninP300-CBP Transcription FactorsHif1αBiologyMelatoninSTAT3chemistry.chemical_compoundHypoxia-Inducible Factor 1-AlphamedicineHuman Umbilical Vein Endothelial CellsHumansp300-CBP Transcription FactorsSTAT3Promoter Regions GeneticTube formationNeovascularization PathologicLiver NeoplasmsCobaltHep G2 Cellshepatocellular carcinomaHypoxia-Inducible Factor 1 alpha SubunitVEGFCell Hypoxiadigestive system diseasesCyclic S-OxidesVascular endothelial growth factorGene Expression Regulation NeoplasticVascular endothelial growth factor AOncologychemistryCancer researchbiology.proteinTranslational Therapeuticsmedicine.drugSignal Transduction
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miR-20b modulates VEGF expression by targeting HIF-1 alpha and STAT3 in MCF-7 breast cancer cells.

2010

MicroRNAs (miRNAs) are small non-coding RNAs that regulate the expression of different genes, including genes involved in cancer progression. A functional link between hypoxia, a key feature of the tumor microenvironment, and miRNA expression has been documented. We investigated whether and how miR-20b can regulate the expression of vascular endothelial growth factor (VEGF) in MCF-7 breast cancer cells under normoxic and hypoxia-mimicking conditions (CoCl(2) exposure). Using immunoblotting, ELISA, and quantitative real-time PCR, we demonstrated that miR-20b decreased VEGF protein levels at 4 and 24 h following CoCl(2) treatment, and VEGF mRNA at 4 h of treatment. In addition, miR-20b reduce…

STAT3 Transcription FactorVascular Endothelial Growth Factor ATime FactorsPhysiologySettore MED/06 - Oncologia MedicaClinical BiochemistryDown-RegulationBreast NeoplasmsBiologyTransfectionchemistry.chemical_compoundmir20b VEGFCell Line TumormicroRNAHumansSTAT3Promoter Regions GeneticG alpha subunitRegulation of gene expressionTumor microenvironmentBinding SitesCell BiologyTransfectionCobaltHypoxia-Inducible Factor 1 alpha SubunitMolecular biologyCell HypoxiaVascular endothelial growth factorGene Expression Regulation NeoplasticMicroRNAsHIF1Achemistrybiology.proteinFemaleRNA InterferenceSignal TransductionJournal of cellular physiology
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SPARC is a new myeloid-derived suppressor cell marker licensing suppressive activities

2019

Myeloid-derived suppressor cells (MDSC) are well-known key negative regulators of the immune response during tumor growth, however scattered is the knowledge of their capacity to influence and adapt to the different tumor microenvironments and of the markers that identify those capacities. Here we show that the secreted protein acidic and rich in cysteine (SPARC) identifies in both human and mouse MDSC with immune suppressive capacity and pro-tumoral activities including the induction of epithelial-to-mesenchymal transition (EMT) and angiogenesis. In mice the genetic deletion of SPARC reduced MDSC immune suppression and reverted EMT. Sparc−/− MDSC were less suppressive overall and the granu…

STAT3 Transcription Factorlcsh:Immunologic diseases. Allergy0301 basic medicineEpithelial-Mesenchymal TransitionAngiogenesisImmunologyneutrophil extracellular trapsNitric Oxide Synthase Type IIInflammationExtracellular TrapsMice03 medical and health sciences0302 clinical medicineImmune systemBreast cancermedicineMyeloid-derived suppressor cellAnimalsHumansImmunology and AllergyOsteonectinOriginal ResearchMice KnockoutMice Inbred BALB CTumor microenvironmentArginaseChemistryNeutrophilNF-kappa B p50 SubunitSPARCNeutrophil extracellular trapsmyeloid-derived suppressor cells030104 developmental biologyCancer researchMyeloid-derived Suppressor CellTumor necrosis factor alphaSignal transductionmedicine.symptomlcsh:RC581-607Neutrophil extracellular trapBiomarkers030215 immunology
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The interleukin-22/STAT3 pathway potentiates expression of inducible nitric-oxide synthase in human colon carcinoma cells.

2007

Inducible nitric-oxide synthase (iNOS) has been identified as a marker and mediator of disease in human colonic inflammation and carcinogenesis. Accordingly, identification of mediators that trigger iNOS in colon carcinoma/epithelial cells is an important topic of current research. Here we demonstrate that interleukin (IL)-22, a newly described member of the IL-10 cytokine family, potently synergizes with interferon (IFN)-gamma for iNOS expression in human DLD-1 colon carcinoma cells. Detection of both IL-22 receptor chains and STAT3 phosphorylation proved robust IL-22 responsiveness of these cells. Short interfering RNA technology identified STAT3 as being crucial for up-regulation of iNOS…

STAT3 Transcription Factormedicine.medical_treatmentNitric Oxide Synthase Type IIBiologymedicine.disease_causeBiochemistryGene Expression Regulation EnzymologicInterleukin 22InterferonmedicineHumansRNA MessengerRNA NeoplasmSTAT3Promoter Regions GeneticMolecular BiologyInflammationInterleukinsNF-kappa BInterleukinCell BiologyTransfectionReceptors InterleukinMolecular biologyNeoplasm ProteinsGene Expression Regulation NeoplasticCytokineSTAT1 Transcription FactorColonic Neoplasmsbiology.proteinCancer researchCytokinesIntercellular Signaling Peptides and ProteinsTumor necrosis factor alphaImmunotherapyCaco-2 CellsCarcinogenesismedicine.drugSignal TransductionThe Journal of biological chemistry
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Leptin and Its Receptor are Overexpressed in Brain Tumors and Correlate with the Degree of Malignancy

2009

Although leptin and its receptor (ObR) have emerged as important cancer biomarkers, the role of the leptin system in brain tumor development remains unknown. We screened 87 human brain tumor biopsies using immunohistochemistry and detected leptin and ObR in 55.2% and 60.9% cases, respectively. In contrast, leptin and ObR were absent in 14 samples of normal brain tissue. The presence of leptin correlated with ObR with overall concordance 80.5%. The leptin/ObR system was highly expressed in glioblastomas and anaplastic astrocytomas, while lower expression of both markers was noted in low-grade astrocytomas and gangliogliomas. The association between leptin/ObR and the degree of tumor malignan…

STAT3 Transcription Factornovel biomarkermedicine.medical_specialtyBlotting WesternBrain tumorFluorescent Antibody TechniqueCell CountBiologyleptinArticlePathology and Forensic MedicineCell Line TumorInternal medicinemedicineHumansleptin receptorProtein kinase BCell ProliferationLeptin receptorBrain NeoplasmsGeneral NeuroscienceLeptindigestive oral and skin physiologyglioblastomaBrainGliomamalignant progressionCell cyclemedicine.diseaseImmunohistochemistryOncogene Protein v-aktglioblastoma; leptin; leptin receptor; malignant progression; novel biomarkerKi-67 AntigenEndocrinologyTumor progressionReceptors LeptinImmunohistochemistryCancer biomarkersNeurology (clinical)hormones hormone substitutes and hormone antagonistsSignal TransductionBrain Pathology
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Novel Signal Transduction Pathways: Analysis of STAT-3 and Rac-1 Signaling in Inflammatory Bowel Disease

2006

Although the precise etiology of inflammatory bowel disease still remains unclear, considerable progress has been made in the identification of novel signal transduction pathways that elucidate the immunopathogenesis involved in the perpetuation of the inflammatory process. Augmented T cell resistance against apoptosis is regarded as a pivotal factor in the pathogenesis, as it impairs mucosal homeostasis and leads to unrestrained accumulation of activated T cells, which subsequently lead to the amplification of the inflammatory response. Therefore novel therapeutic strategies aim at restoring mucosal T cell susceptibility to apoptosis through targeting of signal transduction pathways that a…

STAT3 Transcription Factorrac1 GTP-Binding ProteinT-LymphocytesT cellApoptosisTherapeutic ProcedureAzathioprineBiologyInflammatory bowel diseaseGeneral Biochemistry Genetics and Molecular BiologystatPathogenesisHistory and Philosophy of ScienceAzathioprinemedicineHumansGeneral NeuroscienceInflammatory Bowel Diseasesmedicine.diseasemedicine.anatomical_structureApoptosisImmunologySignal transductionImmunosuppressive AgentsSignal Transductionmedicine.drugAnnals of the New York Academy of Sciences
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