Search results for "stat3"

showing 10 items of 106 documents

The JAK2 pathway is activated in idiopathic pulmonary fibrosis

2018

Background: Idiopathic pulmonary fibrosis (IPF) is the most rapidly progressive and fatal fibrotic disorder, with no curative therapies. The signal transducer and activator of transcription 3 (STAT3) protein is activated in lung fibroblasts and alveolar type II cells (ATII), thereby contributing to lung fibrosis in IPF. Although activation of Janus kinase 2 (JAK2) has been implicated in proliferative disorders, its role in IPF is unknown. The aim of this study was to analyze JAK2 activation in IPF, and to determine whether JAK2/STAT3 inhibition is a potential therapeutic strategy for this disease. Methods and results: JAK2/p-JAK2 and STAT3/pSTAT3 expression was evaluated using quantitative …

0301 basic medicineAdultMaleSTAT3 Transcription FactorIdiopathic pulmonary fibrosisEpithelial cellsLung fibroblastsFibroblast migrationPulmonary fibrosisSTAT303 medical and health sciencesIdiopathic pulmonary fibrosisFibrosishemic and lymphatic diseasesMedicineAnimalsHumansFibroblastAgedlcsh:RC705-779A549 cellCèl·lules epitelialsLungbiologybusiness.industryResearchFibrosi pulmonarlcsh:Diseases of the respiratory systemTransforming growth factor betaFibroblastsJanus Kinase 2Middle Agedrespiratory systemmedicine.diseaseTriterpenesRatsrespiratory tract diseasesEnzyme Activation030104 developmental biologymedicine.anatomical_structureJAK2A549 CellsAlveolar type II epithelial cellsCancer researchbiology.proteinFemalebusinessMyofibroblastSignal Transduction
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The Multifaced Role of STAT3 in Cancer and Its Implication for Anticancer Therapy

2021

Signal transducer and activator of transcription (STAT) 3 is one of the most complex regulators of transcription. Constitutive activation of STAT3 has been reported in many types of tumors and depends on mechanisms such as hyperactivation of receptors for pro-oncogenic cytokines and growth factors, loss of negative regulation, and excessive cytokine stimulation. In contrast, somatic STAT3 mutations are less frequent in cancer. Several oncogenic targets of STAT3 have been recently identified such as c-myc, c-Jun, PLK-1, Pim1/2, Bcl-2, VEGF, bFGF, and Cten, and inhibitors of STAT3 have been developed for cancer prevention and treatment. However, despite the oncogenic role of STAT3 having been…

0301 basic medicineGene isoformSTAT3 Transcription FactorCarcinogenesistumor suppressorPIM1Antineoplastic AgentsReviewBiologyCatalysisstatInorganic ChemistrySTAT3lcsh:Chemistry03 medical and health sciences0302 clinical medicineNeoplasmsDrug DiscoverymedicineAnimalsHumanscancerNeoplasm InvasivenessMolecular Targeted TherapyPhysical and Theoretical ChemistrySTAT3Molecular BiologyTranscription factorlcsh:QH301-705.5SpectroscopyNeovascularization PathologicOrganic ChemistryAlternative splicingtumor promoterCancerGeneral Medicinemedicine.diseaseComputer Science ApplicationsGene Expression Regulation Neoplastic030104 developmental biologylcsh:Biology (General)lcsh:QD1-999030220 oncology & carcinogenesisCancer researchbiology.proteinSTAT proteinInternational Journal of Molecular Sciences
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IL-17 polarization of MAIT cells is derived from the activation of two different pathways

2017

MAIT cells are expanded in salivary glands of patients with Sjogren's syndrome and are IL-17 polarized. IL-7 and IL-23 induce IL-17 production activating two different pathways: IL-7 stimulation induces in fact a significant STAT3 and HIF1alpha upregulation, conversely, IL-23 stimulation significantly induces RORc overexpression in MAIT cells of patients with Sjogren's syndrome.

0301 basic medicineImmunologyStimulationInterleukin-23Mucosal-Associated Invariant T CellsSalivary GlandsSTAT303 medical and health sciencesIL-17; IL-23; IL-7; MAIT cells; RORc; Sjogren's Syndrome; STAT3; Immunology and Allergy; Immunology0302 clinical medicinestomatognathic systemDownregulation and upregulationRAR-related orphan receptor gammaIL-23Interleukin 23HumansImmunology and AllergySTAT3MAIT cellIL-7biologyInterleukin-17MAIT CellsCell biologyRORcIL-17Settore MED/16 - Reumatologia030104 developmental biologySjogren's Syndromebiology.proteinInterleukin 17030215 immunology
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The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension

2021

Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a need for new agents that inhibit pulmonary artery remodeling targeting the main genetic, molecular,…

0301 basic medicineJanus kinase 2 (JAK2)QH301-705.5Hypertension PulmonaryInflammationReviewVascular Remodeling030204 cardiovascular system & hematologyModels BiologicalCatalysisstatInorganic Chemistry03 medical and health sciences0302 clinical medicinemedicine.arterymedicineAnimalsHumanssignal transducer and activator of transcription 3 (STAT3)pulmonary hypertension (PH)Physical and Theoretical ChemistryEndothelial dysfunctionBiology (General)Molecular BiologyQD1-999SpectroscopyJanus Kinasesbiologybusiness.industryOrganic ChemistryJAK-STAT signaling pathwayGeneral Medicinemedicine.diseasePulmonary hypertensionComputer Science ApplicationsSTAT Transcription FactorsChemistry030104 developmental biologyPulmonary arterybiology.proteinCancer researchmedicine.symptombusinessMyofibroblastPlatelet-derived growth factor receptorSignal TransductionInternational Journal of Molecular Sciences
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Mycobacterium tuberculosis Rv2145c Promotes Intracellular Survival by STAT3 and IL-10 Receptor Signaling

2021

Although Mycobacterium tuberculosis (Mtb) is an intracellular pathogen in phagocytic cells, the factors and mechanisms by which they invade and persist in host cells are still not well understood. Characterization of the bacterial proteins modulating macrophage function is essential for understanding tuberculosis pathogenesis and bacterial virulence. Here we investigated the pathogenic role of the Rv2145c protein in stimulating IL-10 production. We first found that recombinant Rv2145c stimulated bone marrow-derived macrophages (BMDMs) to secrete IL-10, IL-6 and TNF-α but not IL-12p70 and to increase the expression of surface molecules through the MAPK, NF-κB, and TLR4 pathways and enhanced …

0301 basic medicineMAPK/ERK pathwayImmunologyMicrobiologySTAT3Mycobacterium tuberculosis03 medical and health sciencesRv2145c0302 clinical medicineImmunology and AllergyMacrophageSecretionOriginal Researchpathogenic rolebiologyMycobacterium smegmatisMycobacterium tuberculosisRC581-607biology.organism_classificationInterleukin 10030104 developmental biology030220 oncology & carcinogenesisIL-10TLR4Immunologic diseases. AllergyIntracellularFrontiers in Immunology
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PTEN status is a crucial determinant of the functional outcome of combined MEK and mTOR inhibition in cancer

2017

AbstractCombined MAPK/PI3K pathway inhibition represents an attractive, albeit toxic, therapeutic strategy in oncology. Since PTEN lies at the intersection of these two pathways, we investigated whether PTEN status determines the functional response to combined pathway inhibition. PTEN (gene, mRNA, and protein) status was extensively characterized in a panel of cancer cell lines and combined MEK/mTOR inhibition displayed highly synergistic pharmacologic interactions almost exclusively in PTEN-loss models. Genetic manipulation of PTEN status confirmed a mechanistic role for PTEN in determining the functional outcome of combined pathway blockade. Proteomic analysis showed greater phosphoprote…

0301 basic medicineMAPK/ERK pathwayPTENRNA interferenceprotein Kinase inhibitorsRNA Small InterferinghumansPhosphoinositide-3 Kinase InhibitorsAnimals; cell line tumor; drug synergism; everolimus; female; humans; Janus Kinase 1; MAP Kinase Kinase Kinases; mice; neoplastic stem cells; PTEN phosphohydrolase; phosphatidylinositol 3-Kinases; protein Kinase inhibitors; proto-oncogene Proteins c-akt; Pyridones; Pyrimidinones; RNA Interference; RNA Small Interfering; STAT3 Transcription Factor; TOR Serine-Threonine KinasesMultidisciplinaryMAPK/PI3K pathway inhibitiononcology MAPK/PI3K pathway inhibitionTOR Serine-Threonine Kinasescell lineMAPK/PI3K inhibition oncology. inhibition. PTEN gene mRNA cancer cell lines MEK/mTORMAP Kinase Kinase KinasesfemaleoncologymTORRNA InterferenceSTAT3 Transcription FactortumormicePyridonesMice NudePyrimidinonesBiologyphosphatidylinositol 3-KinasesSmall InterferingArticle03 medical and health sciencesMediatorSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicinePTENAnimalsPI3K/AKT/mTOR pathwaydrug synergismSettore MED/06 - ONCOLOGIA MEDICAneoplastic stem cellsRPTORCancerJanus Kinase 1medicine.diseaseeverolimusproto-oncogene Proteins c-aktBlockade030104 developmental biologyCancer researchbiology.proteinRNAPTEN phosphohydrolase
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Does bevacizumab impact anti-EGFR therapy efficacy in metastatic colorectal cancer?

2016

IF 5.008; International audience; Anti-EGFR therapy and antiangiogenic therapies are used alone or in combination with chemotherapies to improve survival in metastatic colorectal cancer. However, it is unknown whether pretreatment with antiangiogenic therapy could impact on the efficacy of anti-EGFR therapy. We selected one hundred and twenty eight patients diagnosed with advanced colorectal cancer with a KRAS and NRAS unmutated tumor. These patients were treated with cetuximab or panitumumab alone or with chemotherapy as second or third-line. Univariate and multivariate Cox model analysis were performed to estimate the effect of a previous bevacizumab regimen on progression free survival a…

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyMaleVascular Endothelial Growth Factor AColorectal cancerCetuximabAngiogenesis Inhibitorsmedicine.disease_causeTrialGTP PhosphohydrolasesRas mutations[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsDrug InteractionsAged 80 and overCetuximabPanitumumabAntibodies MonoclonalMiddle Aged3. Good healthErbB ReceptorsOncology030220 oncology & carcinogenesisFemaleKRASColorectal Neoplasms1st-Line treatmentmedicine.drugResearch PaperAdultSTAT3 Transcription Factormedicine.medical_specialtyBevacizumabAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologybevacizumabIrinotecanDisease-Free SurvivalTumor angiogenesisProto-Oncogene Proteins p21(ras)03 medical and health sciencesVEGFRInternal medicineCell Line TumormedicinePanitumumabHumansEndothelial growth-FactorChemotherapyProgression-free survivalAgedbusiness.industry[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMembrane Proteinsmetastatic colon cancerStat-3medicine.diseaseVascular Endothelial Growth Factor Receptor-2IrinotecanRandomized phase-III030104 developmental biologyanti-EGFR therapyFactor receptorCaco-2 Cellsbusiness
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Dibutyltin(IV) and Tributyltin(IV) Derivatives of meso-Tetra(4 sulfonatophenyl)porphine Inhibit the Growth and the Migration of Human Melanoma Cells.

2019

Melanoma is the most aggressive and deadly form of skin cancer, which is largely due to its propensity to metastasize. Therefore, with the aim to inhibit the growth and the metastatic dissemination of melanoma cells and to provide a novel treatment option, we studied the effects of the melanoma treatment with two organotin(IV) complexes of the meso-tetra(4-sulfonato-phenyl)porphine, namely (Bu2Sn)2TPPS and (Bu3Sn)4TPPS. In particular, we showed that nanomolar concentrations of (Bu2Sn)2TPPS and (Bu3Sn)4TPPS are sufficient to inhibit melanoma cell growth, to increase the expression of the full-length poly (ADP-ribose) polymerase (PARP-1), to induce the cell cycle arrest respectively at G2/M a…

0301 basic medicinePorphyrinsCellAntineoplastic AgentsApoptosisorganotin(IV)migrationArticleBRAF03 medical and health sciences0302 clinical medicineCyclin D1Cell MovementCell Line Tumormelanoma; organotin(IV); cellular growth; BRAF; cell cycle; migrationmedicinemelanomaHumansSTAT3Cell ProliferationDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryMelanomaCell migrationCell Cycle CheckpointsGeneral Medicinecellular growthCell cyclemedicine.disease030104 developmental biologymedicine.anatomical_structureFocal Adhesion Kinase 1030220 oncology & carcinogenesisbiology.proteinCancer researchcell cycleSkin cancerSignal Transduction
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Nuclear Factor Kappa B Signaling Complexes in Acute Inflammation.

2020

[Significance]: Nuclear factor kappa B (NF-κB) is a master regulator of the inflammatory response and represents a key regulatory node in the complex inflammatory signaling network. In addition, selective NF-κB transcriptional activity on specific target genes occurs through the control of redox-sensitive NF-κB interactions.

0301 basic medicineRedox signalingPhysiologyClinical BiochemistryRepressorCREBInteractomeBiochemistry03 medical and health sciencesCoactivatorHumansSTAT3Transcription factorMolecular BiologyGeneral Environmental ScienceInflammation030102 biochemistry & molecular biologybiologyChemistryActivator (genetics)NF-kappa BCell Biology3. Good healthCell biology030104 developmental biologyGene Expression RegulationMultiprotein ComplexesAcute DiseaseSTAT proteinbiology.proteinGeneral Earth and Planetary SciencesDisease SusceptibilitySignaling complexesCarrier ProteinsBiomarkersProtein BindingSignal TransductionAntioxidantsredox signaling
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Inhibition of STAT3 with the generation 2.5 antisense oligonucleotide, AZD9150, decreases neuroblastoma tumorigenicity and increases chemosensitivity

2017

Abstract Purpose: Neuroblastoma is a pediatric tumor of peripheral sympathoadrenal neuroblasts. The long-term event-free survival of children with high-risk neuroblastoma is still poor despite the improvements with current multimodality treatment protocols. Activated JAK/STAT3 pathway plays an important role in many human cancers, suggesting that targeting STAT3 is a promising strategy for treating high-risk neuroblastoma. Experimental Design: To evaluate the biologic consequences of specific targeting of STAT3 in neuroblastoma, we assessed the effect of tetracycline (Tet)-inducible STAT3 shRNA and the generation 2.5 antisense oligonucleotide AZD9150 which targets STAT3 in three representat…

0301 basic medicineSTAT3 Transcription FactorCancer Researchmedicine.disease_causeSmall hairpin RNA03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineNeuroblastomaCell Line TumorOligonucleotidemedicineSTAT3CarcinogenesiCell ProliferationCisplatinAntineoplastic Combined Chemotherapy ProtocolbiologyCell growthAnimalCancerApoptosiOligonucleotides Antisensemedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation Neoplastic030104 developmental biologyOncologyCell culture030220 oncology & carcinogenesisCancer researchbiology.proteinCisplatinCarcinogenesismedicine.drugHuman
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