Search results for " NF-κB"

showing 10 items of 17 documents

Tumor-Derived Prostaglandin E2 Promotes p50 NF-κB-Dependent Differentiation of Monocytic MDSCs

2020

Abstract Myeloid-derived suppressor cells (MDSC) include immature monocytic (M-MDSC) and granulocytic (PMN-MDSC) cells that share the ability to suppress adaptive immunity and to hinder the effectiveness of anticancer treatments. Of note, in response to IFNγ, M-MDSCs release the tumor-promoting and immunosuppressive molecule nitric oxide (NO), whereas macrophages largely express antitumor properties. Investigating these opposing activities, we found that tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation of p50 NF-κB in M-MDSCs, diverting their response to IFNγ toward NO-mediated immunosuppression and reducing TNFα expression. At the genome level, p50 NF-κB promoted binding …

0301 basic medicineCancer ResearchCellular differentiationProstaglandin E2 receptormedicine.medical_treatmentMelanoma ExperimentalApoptosisSettore MED/08 - Anatomia PatologicaNitric OxideDinoprostoneMonocytesInterferon-gammaMice03 medical and health sciences0302 clinical medicineImmune systemOxytocicsImmune ToleranceTumor Cells CulturedmedicineAnimalsHumansProstaglandin E2Cell ProliferationChemistryMyeloid-Derived Suppressor CellsNF-kappa B p50 SubunitCell DifferentiationImmunotherapyAcquired immune systemPancreatic Neoplasms030104 developmental biologyOncologyp50 NF-κB differentiation of monocytic MDSC.030220 oncology & carcinogenesisMyeloid-derived Suppressor CellCancer researchTumor necrosis factor alphaColorectal Neoplasmsmedicine.drugCancer Research
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Potential Therapeutic Applications of MDA-9/Syntenin-NF-κB-RKIP Loop in Human Liver Carcinoma

2019

Background Overexpression of MDA-9/Syntenin occurs in multiple human cancer cell lines and is associated with higher grade of tumor classification, invasiveness and metastasis. In some cases, its role in cancer biology depends on relationships between MDA-9/Syntenin and NF-κB. Objective This study aims to analyze the presence of a regulation loop like that between MDA-9/Syntenin - NF-κB - RKIP in human liver carcinoma. Methods Transient transfection was performed with siRNA anti-MDA-9/Syntenin. Expression of different factors was evaluated by Real time-PCR and Western blotting, while NF-κB activation by TransAM assay. Invasion capacity was analyzed by Matrigel Invasion Assay and the effects…

0301 basic medicineMDA-9/Syntenin NF-κB RKIP drug targets HA22T/VGH Hep3B HepG2Carcinoma HepatocellularCurcuminSynteninsPhosphatidylethanolamine Binding ProteinBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationAntineoplastic Combined Chemotherapy ProtocolsHumansGene silencingNeoplasm InvasivenessViability assayMolecular BiologyCell growthMatrigel Invasion AssayLiver NeoplasmsNF-kappa BNF-κBHep G2 CellsGeneral MedicineNeoplasm ProteinsBlot030104 developmental biologychemistryDoxorubicinCell cultureSettore BIO/14 - FarmacologiaCancer researchMolecular MedicineSignal Transduction030215 immunologyCurrent Molecular Medicine
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The murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated trans…

2017

The type I interferon (IFN) response is imperative for the establishment of the early antiviral immune response. Here we report the identification of the first type I IFN antagonist encoded by murine cytomegalovirus (MCMV) that shuts down signaling following pattern recognition receptor (PRR) sensing. Screening of an MCMV open reading frame (ORF) library identified M35 as a novel and strong negative modulator of IFNβ promoter induction following activation of both RNA and DNA cytoplasmic PRR. Additionally, M35 inhibits the proinflammatory cytokine response downstream of Toll-like receptors (TLR). Using a series of luciferase-based reporters with specific transcription factor binding sites, …

0301 basic medicineMuromegalovirusPhysiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundMiceWhite Blood Cells0302 clinical medicineCell SignalingTranscription (biology)InterferonAnimal CellsImmune PhysiologyMedicine and Health SciencesMembrane Receptor SignalingBiology (General)Enzyme-Linked ImmunoassaysReceptorConnective Tissue CellsbiologyToll-Like ReceptorsPattern recognition receptorNF-kappa BImmune Receptor SignalingEnzymesThe murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated transcription.Connective TissueReceptors Pattern RecognitionCytomegalovirus InfectionsInterferon Type ISignal transductionCellular TypesAnatomyBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.OxidoreductasesLuciferasemedicine.drugProtein BindingSignal TransductionResearch ArticleViral proteinQH301-705.5Immune CellsImmunologyResearch and Analysis MethodsTransfectionMicrobiology03 medical and health sciencesViral ProteinsMuromegalovirusVirologyGeneticsmedicineAnimalsImmunoassaysMolecular Biology TechniquesMolecular BiologyBlood CellsMacrophagesBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Biology and Life SciencesProteinsNF-κBInterferon-betaCell BiologyRC581-607Fibroblastsbiology.organism_classificationMolecular biology030104 developmental biologyBiological TissuechemistryEnzymologyImmunologic TechniquesParasitologyInterferonsImmunologic diseases. AllergySpleen030215 immunology
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Melatonin reduces inflammatory response in human intestinal epithelial cells stimulated by interleukin‐1β

2019

Melatonin is the main secretory product of the pineal gland, and it is involved in the regulation of periodic events. A melatonin production independent of the photoperiod is typical of the gut. However, the local physiological role of melatonin at the intestinal tract is poorly characterized. In this study, we evaluated the anti-inflammatory activities of melatonin in an in vitro model of inflamed intestinal epithelium. To this purpose, we assessed different parameters usually associated with intestinal inflammation using IL-1 beta-stimulated Caco-2 cells. Differentiated monolayers of Caco-2 cells were preincubated with melatonin (1 nmol/L-50 mu mol/L) and then exposed to IL-1 beta. After …

0301 basic medicineendocrine systemmedicine.medical_specialtyantioxidantDNA damageInterleukin-1betainflammatory bowel diseasesdietary supplementsMelatonin03 medical and health sciencesPineal gland0302 clinical medicineEndocrinologyCell surface receptorSettore BIO/10 - BiochimicaInternal medicinemedicineHumansMelatoninInflammationN-acetyl-5-methoxy-tryptamineInterleukin-6Chemistryantioxidants; dietary supplements; DNA damage; DNA methylation; inflammatory bowel diseases; N-acetyl-5-methoxy-tryptamine; NF-κB activationInterleukin-8AntagonistCell DifferentiationEpithelial CellsDNA MethylationSettore CHIM/08 - Chimica FarmaceuticaIntestinal epitheliumIntestinesSettore BIO/18 - Geneticaantioxidants030104 developmental biologyEndocrinologymedicine.anatomical_structureNF-κB activationCyclooxygenase 2dietary supplementParacellular transportDNA damageCaco-2 CellsLuzindolehormones hormone substitutes and hormone antagonists030217 neurology & neurosurgerySignal Transductionmedicine.drugJournal of Pineal Research
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The role of extracellular calcium in bone metastasis

2016

AbstractThis review summarizes the role of extracellular calcium, as found present in the bone tissue, in the process of bone metastasis.

0301 basic medicinelcsh:Diseases of the musculoskeletal systemIGF insulin-like growth factorPGE-2 prostaglandin E-2Bone tissueFibroblast growth factorM-CSF macrophage colony-stimulating factorPDGF platelet-derived growth factorBone remodelingSK3 small conductance calcium-activated potassium channel 30302 clinical medicineERK extracellular signal-regulated kinaseTGFβ transforming growth factor betaBMP's bone morphogenetic proteinsbiologyAKT AKT8 virus oncogene cellular homologBone metastasislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenshumanitiescAMP cyclic adenosine monophosphatemedicine.anatomical_structureOncologyRANKL030220 oncology & carcinogenesisIon channelsCaSR calcium-sensing receptorPTHrP parathyroid hormone-related proteinPlatelet-derived growth factor receptorResearch PaperTRP transient receptor potentialmedicine.medical_specialtychemistry.chemical_elementCalciumRANKL receptor activator of NF-κB ligandlcsh:RC254-28203 medical and health sciencesPLC phospholipase CInternal medicinemedicineExtracellularCaSRET-1 endothelin-1PTEN phosphatase and tensin homolog deleted on chromosome 10business.industryBone metastasismedicine.diseaseFGF fibroblast growth factor030104 developmental biologyEndocrinologyPSA prostate specific antigenchemistryCOPD chronic obstructive pulmonary diseasebiology.proteinCancer researchJNK jun N-terminal kinasePKA protein kinase ARANK receptor activator of NF-κBCalciumlcsh:RC925-935businessMAPK mitogen-activated protein kinaseJournal of Bone Oncology
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Resveratrol Interferes with IL1-β-Induced Pro-Inflammatory Paracrine Interaction between Primary Chondrocytes and Macrophages

2016

International audience; State of the art. Osteoarthritis (OA) is a chronic articular disease characterized by cartilage degradation and osteophyte formation. OA physiopathology is multifactorial and involves mechanical and hereditary factors. So far, there is neither preventive medicine to delay cartilage breakdown nor curative treatment. Objectives. To investigate pro-inflammatory paracrine interactions between human primary chondrocytes and macrophages following interleukin-1-β (IL-1β) treatment; to evaluate the molecular mechanism responsible for the inhibitory effect of resveratrol. Results. The activation of NF-κB in chondrocytes by IL-1β induced IL-6 secretion. The latter will then ac…

0301 basic medicinemedicine.medical_specialtyTime Factors[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionInterleukin-1betalcsh:TX341-641InflammationmacrophageResveratrolresveratrolChondrocyteArticleNF-κBSTAT303 medical and health scienceschemistry.chemical_compoundParacrine signallingChondrocytesInternal medicineStilbenesmedicineMacrophageHumansSecretionCells CulturedInflammationNutrition and DieteticsCartilageMacrophagesAnti-Inflammatory Agents Non-SteroidalNF-κBIL1-β; chondrocyte; macrophage; NF-κB; STAT3; resveratrolCoculture TechniquesCell biology030104 developmental biologyEndocrinologymedicine.anatomical_structurechemistrychondrocytemedicine.symptomIL1-βlcsh:Nutrition. Foods and food supplyBiomarkersFood ScienceNutrients
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HSP60 activity on human bronchial epithelial cells

2017

HSP60 has been implicated in chronic inflammatory disease pathogenesis, including chronic obstructive pulmonary disease (COPD), but the mechanisms by which this chaperonin would act are poorly understood. A number of studies suggest a role for extracellular HSP60, since it can be secreted from cells and bind Toll-like receptors; however, the effects of this stimulation have never been extensively studied. We investigated the effects (pro- or anti-inflammatory) of HSP60 in human bronchial epithelial cells (16-HBE) alone and in comparison with oxidative, inflammatory, or bacterial challenges. 16-HBE cells were cultured for 1–4 h in the absence or presence of HSP60, H2O2, lipopolysaccharide (…

0301 basic medicinep38αSettore BIO/17 - IstologiaLipopolysaccharidep38 mitogen-activated protein kinasesImmunologyStimulationBronchip38 Mitogen-Activated Protein KinasesERK1Cell LinePathogenesisMitochondrial Proteins03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOriginal Research ArticlesHumansImmunology and AllergyCOPDInterleukin 8Protein kinase AReceptor16-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; TLR-4; p38αPharmacologyIL-8Settore BIO/16 - Anatomia UmanaInterleukin-8JNK1NF-κB p65 subunitEpithelial CellsTLR-4Chaperonin 60MyD88Interleukin-1016-HBEToll-Like Receptor 416-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; p38α; TLR-4; Immunology and Allergy; Immunology; PharmacologyInterleukin 10030104 developmental biologychemistry030220 oncology & carcinogenesisIL-10Cancer researchCREB1NF-κB p65 subunitHSP60p38α
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NF-κB pathway activators as potential ageing biomarkers: targets for new therapeutic strategies

2013

Chronic inflammation is a major biological mechanism underpinning biological ageing process and age-related diseases. Inflammation is also the key response of host defense against pathogens and tissue injury. Current opinion sustains that during evolution the host defense and ageing process have become linked together. Thus, the large array of defense factors and mechanisms linked to the NF-κB system seem to be involved in ageing process. This concept leads us in proposing inductors of NF-κB signaling pathway as potential ageing biomarkers. On the other hand, ageing biomarkers, represented by biological indicators and selected through apposite criteria, should help to characterize biologica…

AgingBiological ageInflammatory network and its effects in ageingImmunologyLarge arrayReviewWorking hypothesisBiological ageing processchemistry.chemical_compoundBiological ageing process Inflammatory network and its effects in ageing NF-κB signaling pathway as hub of inflammatory ageing network Inflammatory biomarkersSettore MED/05 - Patologia ClinicaMedicineSettore MED/04 - Patologia Generalebusiness.industryMechanism (biology)NF-κBInflammatory biomarkersRisk factor (computing)NF-κB signaling pathway as hub of inflammatory ageing networkInflammatory biomarkersAgeingchemistryAgeingImmunologybusinessNeuroscienceImmunity & Ageing
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Patterns of Innate or Acquired Resistance to Anticancer Drugs: Our Experience to Overcome It

2021

Drug resistance, which is often of a multiple type, can be defined as the ability of cancer cells to obtain resistance to both conventional and novel chemotherapy agents. It remains a major problem to solve in cancer therapy. The mechanisms of resistance are multifactorial, and in our cellular models of acute myeloid leukemia, hepatocellular carcinoma, and triple-negative breast cancer, it involves the NF-κB pathway. In our opinion, multitarget molecules can be considered as privileged compounds capable of attacking and reversing the resistant phenotype. In the phenomena of both innate and acquired drug resistance that we have been studying since 1998 to today and up to 2016 under the guida…

Cancer ResearchAntineoplastic AgentsApoptosisPhosphatidylethanolamine Binding ProteinDrug resistanceMetastasisBreast cancerdrug resistance P-glycoprotein IAP NF-κBNeoplasmsHumansMedicineATP Binding Cassette Transporter Subfamily B Member 1Transcription factorYY1 Transcription FactorP-glycoproteinbiologybusiness.industryKinaseNF-kappa BMyeloid leukemiamedicine.diseaseDrug Resistance NeoplasmCancer cellSettore BIO/14 - Farmacologiabiology.proteinCancer researchbusinessCritical Reviews™ in Oncogenesis
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Synthesis, In Vitro and In Silico Analysis of New Oleanolic Acid and Lupeol Derivatives against Leukemia Cell Lines: Involvement of the NF-κB Pathway

2022

Oleanolic acid (OA) and Lupeol (LU) belong to the class of natural triterpenes and are endowed with a wide range of biological activities, including cytotoxicity toward several cancer cell lines. In this context, we investigated a set of compounds obtained from the two natural precursors for the cytotoxicity against leukemia HL60 cells and the multidrug-resistant (MDR) variant HL60R. Six new semi-synthetic triterpenes have been synthetized, fully characterized, and were investigated together with other triterpenes compounds for their pharmacological mechanism of action. The interaction of the more cytotoxic compounds with the nuclear factor kappa B (NF-κB) pathway has been also evalua…

CatalysisCell LineInorganic ChemistryNeoplasmsHumansantitumor activityNF-kBPhysical and Theoretical ChemistryMolecular BiologySpectroscopyLeukemiaHL60ROrganic ChemistryNF-kappa BLupeolOleanolic acidSettore CHIM/06 - Chimica OrganicaGeneral MedicineSettore CHIM/08 - Chimica FarmaceuticaTriterpenesComputer Science ApplicationsOleanolic acid; Lupeol; HL60; HL60R; antitumor activity; NF-κB; dockingHL60dockingSettore BIO/14 - FarmacologiaPentacyclic TriterpenesInternational Journal of Molecular Sciences
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