Search results for "NF-"

showing 10 items of 461 documents

Marine Actinomycetes-Derived Secondary Metabolites Overcome TRAIL-Resistance via the Intrinsic Pathway through Downregulation of Survivin and XIAP

2020

Resistance of cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis represents the major hurdle to the clinical use of TRAIL or its derivatives. The discovery and development of lead compounds able to sensitize tumor cells to TRAIL-induced cell death is thus likely to overcome this limitation. We recently reported that marine actinomycetes&rsquo

0301 basic medicineAquatic OrganismsProgrammed cell deathCell SurvivalSurvivinDown-RegulationSecondary MetabolismX-Linked Inhibitor of Apoptosis ProteinTRAILJurkat cellsArticleTNF-Related Apoptosis-Inducing LigandJurkat Cells03 medical and health sciences0302 clinical medicinemarine actinomycetesDownregulation and upregulationDrug DiscoveryOxazinesSurvivinHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyFADDBenzopyreneslcsh:QH301-705.5ComputingMilieux_MISCELLANEOUSCaspase 8therapybiologyChemistryProdigiosinQuinonesapoptosisGeneral MedicineHCT116 Cells3. Good healthXIAPActinobacteria030104 developmental biologylcsh:Biology (General)Drug Resistance NeoplasmApoptosis030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchGene DeletionCells
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Context-Dependent Role of NF-κB Signaling in Primary Liver Cancer—from Tumor Development to Therapeutic Implications

2019

Chronic inflammatory cell death is a major risk factor for the development of diverse cancers including liver cancer. Herein, disruption of the hepatic microenvironment as well as the immune cell composition are major determinants of malignant transformation and progression in hepatocellular carcinomas (HCC). Considerable research efforts have focused on the identification of predisposing factors that promote induction of an oncogenic field effect within the inflammatory liver microenvironment. Among the most prominent factors involved in this so-called inflammation-fibrosis-cancer axis is the NF-κB pathway. The dominant role of this pathway for malignant transformation and progression…

0301 basic medicineCancer ResearchCell typechronic inflammationContext (language use)Reviewlcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicineImmune systemMedicinebusiness.industryhepatocarcinogenesishepatocellular carcinomalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseNf κb signaling030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomaNF-κB signalingCancer researchbusinessLiver cancerPrimary liver cancerCancers
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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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Parthenolide and DMAPT exert cytotoxic effects on breast cancer stem-like cells by inducing oxidative stress, mitochondrial dysfunction and necrosis

2016

Triple-negative breast cancers (TNBCs) are aggressive forms of breast carcinoma associated with a high rate of recidivism. In this paper, we report the production of mammospheres from three lines of TNBC cells and demonstrate that both parthenolide (PN) and its soluble analog dimethylaminoparthenolide (DMAPT) suppressed this production and induced cytotoxic effects in breast cancer stem-like cells, derived from dissociation of mammospheres. In particular, the drugs exerted a remarkable inhibitory effect on viability of stem-like cells. Such an effect was suppressed by N-acetylcysteine, suggesting a role of reactive oxygen species (ROS) generation in the cytotoxic effect. Instead z-VAD, a ge…

0301 basic medicineCancer ResearchNecrosismedicine.disease_causeCancer -- Treatmentchemistry.chemical_compoundOnium CompoundsMedicineCytotoxic T cellBreast -- CancerMembrane Potential Mitochondrialchemistry.chemical_classificationSuperoxideMitochondrial DNAMitochondriaNeoplastic Stem CellsFemaleOriginal Articlemedicine.symptomOligopeptidesSesquiterpenesCell SurvivalNF-E2-Related Factor 2ImmunologyBreast NeoplasmsReal-Time Polymerase Chain Reaction03 medical and health sciencesCellular and Molecular NeuroscienceDownregulation and upregulationCell Line TumorHumansParthenolideparthenolide cancer stem cell triple-negative breast cancer reactive oxygen species nuclear factor erythroid 2-related factor 2Fluorescent DyesReactive oxygen speciesbusiness.industryAcetophenonesNADPH OxidasesCell BiologyCell nuclei -- AbnormalitiesOxidative Stress030104 developmental biologychemistryApocyninImmunologyCancer researchReactive Oxygen SpeciesbusinessOxidative stressTranscription FactorsCell Death & Disease
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The secreted protein acidic and rich in cysteine is a critical mediator of cell death program induced by WIN/TRAIL combined treatment in osteosarcoma…

2015

Abstract Secreted protein acidic and rich in cysteine (SPARC) is a multi-functional protein which modulates cell-cell and cell-matrix interactions. In cancer cells, SPARC behaves as a tumor promoter in a number of tumors, but it can also act as a tumor suppressor factor. Our previous results showed that the synthetic cannabinoid WIN55,212-2 (WIN), a potent cannabinoid receptor agonist, is able to sensitize osteosarcoma MG63 cells to TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis which is accompanied with endoplasmic reticulum (ER)-stress induction and the increase in autophagic markers. In the present investigation, we studied the role of SPARC in WIN/TRAIL-induced apoptosi…

0301 basic medicineCancer ResearchProgrammed cell deathCell SurvivalMorpholinesCellSPARC cannabinoids osteosarcoma apoptosis caspase-8 activationApoptosisBone NeoplasmsBiologyNaphthalenesTNF-Related Apoptosis-Inducing Ligand03 medical and health sciences0302 clinical medicineProtein DomainsSettore BIO/10 - BiochimicaCell Line TumormedicineCytotoxic T cellHumansOsteonectinGene SilencingCaspase 8OsteosarcomaOncogeneCell DeathEndoplasmic reticulumCell MembraneCell cycleEndoplasmic Reticulum StressCell biologyBenzoxazines030104 developmental biologymedicine.anatomical_structureOncologyApoptosis030220 oncology & carcinogenesisCancer cellRNA InterferenceInternational journal of oncology
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Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling

2017

The pathogenesis of chronic lymphocytic leukemia (CLL) has been linked to constitutive NF-κB activation but the underlying mechanisms are poorly understood. Here we show that alternative splicing of the negative regulator of NF-κB and tumor suppressor gene CYLD regulates the pool of CD5+ B cells through sustained canonical NF-κB signaling. Reinforced canonical NF-κB activity leads to the development of B1 cell-associated tumor formation in aging mice by promoting survival and proliferation of CD5+ B cells, highly reminiscent of human B-CLL. We show that a substantial number of CLL patient samples express sCYLD, strongly implicating a role for it in human B-CLL. We propose that our new CLL-l…

0301 basic medicineCancer ResearchTumor suppressor geneCell SurvivalRNA SplicingChronic lymphocytic leukemia2720 Hematology610 Medicine & healthBiologyCD5 Antigenslaw.inventionPathogenesisMice03 medical and health sciencesimmune system diseaseslawhemic and lymphatic diseasesmedicineAnimalsHumans10239 Institute of Laboratory Animal Science1306 Cancer ResearchGenes Tumor SuppressorGeneCell ProliferationB-LymphocytesAlternative splicingNF-kappa BUbiquitinationHematologymedicine.diseaseLeukemia Lymphocytic Chronic B-CellDeubiquitinating Enzyme CYLDLeukemia030104 developmental biologyOncologyImmunologyCancer research570 Life sciences; biologySuppressor2730 OncologyCD5Signal TransductionLeukemia
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Ginkgo biloba induces different gene expression signatures and oncogenic pathways in malignant and non-malignant cells of the liver

2018

Ginkgo biloba (EGb761) is a widely used botanical drug. Several reports indicate that EGb761 confers preventive as well as anti-tumorigenic properties in a variety of tumors, including hepatocellular carcinoma (HCC). We here evaluate functional effects and molecular alterations induced by EGb761 in hepatoma cells and non-malignant hepatocytes. Hepatoma cell lines, primary human HCC cells and immortalized human hepatocytes (IH) were exposed to various concentrations (0-1000 μg/ml) of EGb761. Apoptosis and proliferation were evaluated after 72h of EGb761 exposure. Response to oxidative stress, tumorigenic properties and molecular changes were further investigated. While anti-oxidant effects w…

0301 basic medicineCarcinogenesisApoptosismedicine.disease_causeBiochemistryAntioxidantsTranscriptome0302 clinical medicineCell SignalingAnimal CellsMedicine and Health SciencesCellular Stress ResponsesCultured Tumor CellsMultidisciplinaryCell DeathbiologyGinkgo bilobaTOR Serine-Threonine KinasesLiver NeoplasmsQRLiverOncologyCell Processes030220 oncology & carcinogenesisHepatocellular carcinomaMedicineBiological CulturesCellular TypesAnatomyResearch ArticleSignal TransductionCarcinoma HepatocellularNF-E2-Related Factor 2ScienceResearch and Analysis MethodsCell Line03 medical and health sciencesmedicineHumansCell ProliferationOncogenic SignalingPlant ExtractsBiology and Life SciencesGinkgo bilobaCell BiologyCell Culturesbiology.organism_classificationmedicine.diseaseOxidative Stress030104 developmental biologyCell cultureApoptosisCancer cellHepatocytesCancer researchHepatoma CellsTranscriptomeCarcinogenesisOxidative stressPLOS ONE
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Chemopreventive Property of Sencha Tea Extracts towards Sensitive and Multidrug-Resistant Leukemia and Multiple Myeloma Cells

2020

The popular beverage green tea possesses chemopreventive activity against various types of tumors. However, the effects of its chemopreventive effect on hematological malignancies have not been defined. In the present study, we evaluated antitumor efficacies of a specific green tea, sencha tea, on sensitive and multidrug-resistant leukemia and a panel of nine multiple myelomas (MM) cell lines. We found that sencha extracts induced cytotoxicity in leukemic cells and MM cells to different extents, yet its effect on normal cells was limited. Furthermore, sencha extracts caused G2/M and G0/G1 phase arrest during cell cycle progression in CCRF/CEM and KMS-12-BM cells, respectively. Specifically,…

0301 basic medicineCell Survivalnatural productsgreen tealcsh:QR1-502Cell morphologychemotherapyBiochemistryArticlelcsh:Microbiologyfunctional foodPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCell Line TumorHumansCytotoxicityMolecular BiologyProtein kinase BcatechinsPI3K/AKT/mTOR pathwaypolyphenolsCell ProliferationMembrane Potential MitochondrialLeukemiadrug resistanceTeaPlant ExtractsChemistryCell growthCell CycleNF-kappa BCell cycleAntineoplastic Agents PhytogenicDrug Resistance MultipleGene Expression Regulation Neoplastic030104 developmental biologyDrug Resistance NeoplasmApoptosisCell culture030220 oncology & carcinogenesisflavonoidsCancer researchmicroarray analysisMultiple MyelomaReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSignal TransductionBiomolecules
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The Role of Nrf2 and PPARγ in the Improvement of Oxidative Stress in Hypertension and Cardiovascular Diseases

2020

Reactive oxygen species are an important element of redox regulation in cells and tissues. During physiological processes, molecules undergo chemical changes caused by reduction and oxidation reactions. Free radicals are involved in interactions with other molecules, leading to oxidative stress. Oxidative stress works two ways depending on the levels of oxidizing agents and products. Excessive action of oxidizing agents damages biomolecules, while a moderate physiological level of oxidative stress (oxidative eustress) is necessary to control life processes through redox signaling required for normal cellular operation. High levels of reactive oxygen species (ROS) mediate pathological change…

0301 basic medicineCell signalingNF-E2-Related Factor 2PhysiologyBlood PressureReviewOxidative phosphorylationmedicine.disease_cause03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwaychemistry.chemical_classificationReactive oxygen speciesKelch-Like ECH-Associated Protein 1ChemistryGeneral MedicineKEAP1Antioxidant Response ElementsNFE2L2Cell biologyPPAR gammaOxidative Stress030104 developmental biologyCardiovascular DiseasesHypertensionReactive Oxygen Species030217 neurology & neurosurgeryOxidative stressSignal TransductionPhysiological Research
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NFATc1 releases BCL6-dependent repression of CCR2 agonist expression in peritoneal macrophages fromSaccharomyces cerevisiaeinfected mice

2016

The link between the extensive usage of calcineurin (CN) inhibitors cyclosporin A and tacrolimus (FK506) in transplantation medicine and the increasing rate of opportunistic infections within this segment of patients is alarming. Currently, how peritoneal infections are favored by these drugs, which impair the activity of several signaling pathways including the Ca(++) /CN/NFAT, Ca(++) /CN/cofilin, Ca(++) /CN/BAD, and NF-κB networks, is unknown. Here, we show that Saccharomyces cerevisiae infection of peritoneal resident macrophages triggers the transient nuclear translocation of NFATc1β isoforms, resulting in a coordinated, CN-dependent induction of the Ccl2, Ccl7, and Ccl12 genes, all enc…

0301 basic medicineChemokineReceptors CCR2Calcineurin InhibitorsImmunologySaccharomyces cerevisiaeOpportunistic InfectionsCCL7MonocytesMice03 medical and health sciences0302 clinical medicineCyclosporin aAnimalsProtein IsoformsImmunology and AllergyChemokine CCL7Promoter Regions GeneticCCL12Transcription factorChemokine CCL2NFATC Transcription FactorsbiologyCalcineurinNF-kappa BNFATNFATC Transcription FactorsMonocyte Chemoattractant Proteins3. Good healthCalcineurinProtein Transport030104 developmental biology030220 oncology & carcinogenesisMacrophages PeritonealProto-Oncogene Proteins c-bcl-6biology.proteinCancer researchEuropean Journal of Immunology
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