Search results for "Tumor necrosis factor-alpha"

showing 10 items of 504 documents

Redistribution of CD95, DR4 and DR5 in rafts accounts for the synergistic toxicity of resveratrol and death receptor ligands in colon carcinoma cells.

2004

The natural phytoalexin resveratrol (3, 5, 4'-trihydroxystilbene) exhibits both chemopreventive and antitumor activities through a variety of mechanisms. We have shown previously that resveratrol-induced apoptosis of a human colon cancer cell line involved the redistribution of CD95 (Fas/Apo-1) into lipid rafts. Here, we show that, in colon cancer cells that resist to resveratrol-induced apoptosis, the polyphenol also induces a redistribution of death receptors into lipid rafts. This effect sensitizes these tumor cells to death receptor-mediated apoptosis. In resveratrol-treated cells, tumor necrosis factor (TNF), anti-CD95 antibodies and TNF-related apoptosis-inducing ligand (TRAIL) activa…

Cancer ResearchNystatinTime FactorsApoptosisResveratrolmedicine.disease_causeLigandsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundStilbenesReceptorLipid raftCaspaseMembrane GlycoproteinsbiologyFas receptorFlow CytometryLipidsMitochondriaProto-Oncogene Proteins c-bcl-2CaspasesColonic Neoplasmslipids (amino acids peptides and proteins)Tumor necrosis factor alphaSignal Transductionmedicine.medical_specialtyBlotting WesternTransfectionMembrane MicrodomainsInternal medicineCell Line TumorGeneticsmedicineHumansfas ReceptorMolecular BiologyTumor Necrosis Factor-alphaCarcinomaLipid MetabolismAntineoplastic Agents PhytogenicReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologychemistryApoptosisResveratrolCancer researchbiology.proteinCarcinogenesisApoptosis Regulatory ProteinsOncogene
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Histone deacetylase inhibition by valproic acid down-regulates c-FLIP/CASH and sensitizes hepatoma cells towards CD95-and TRAIL receptor-mediated apo…

2005

Hepatocellular carcinoma (HCC) is highly resistant to chemotherapy, leading to a poor prognosis of advanced disease. Inhibitors of histone deacetylase (HDACi) induce re-differentiation in tumor cells and thereby re-establish sensitivity towards apoptotic stimuli. HDACi are entering the clinical stage of tumor treatment, and several substances are currently being tested in clinical trials to prove their efficacy in the treatment of leukemias and solid tumors. In this study, we investigated the impact of the HDACi valproic acid (VA) on TRAIL- and CD95-mediated apoptosis in hepatoma cells, as well as its sensitizing effect on a chemotherapeutic agent. Treatment of HepG2 cells with VA increased…

Cancer ResearchProgrammed cell deathCarcinoma Hepatocellularmedicine.medical_treatmentCellCASP8 and FADD-Like Apoptosis Regulating ProteinDown-RegulationCaspase 3ApoptosisBiologyReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansfas ReceptorEpirubicinChemotherapyMembrane GlycoproteinsCaspase 3Tumor Necrosis Factor-alphaValproic AcidLiver NeoplasmsIntracellular Signaling Peptides and ProteinsGeneral MedicineCell cycleFas receptorHistone Deacetylase Inhibitorsmedicine.anatomical_structureOncologyApoptosisDrug Resistance NeoplasmCaspasesCancer researchHistone deacetylaseApoptosis Regulatory Proteins
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SGK-1 protects kidney cells against apoptosis induced by ceramide and TNF-α

2015

AbstractCeramide regulates several different cellular responses including mechanisms leading to apoptosis. Serum- and glucocorticoid-inducible protein kinase (SGK)-1 is a serine threonine kinase, which activates survival pathways in response to stress stimuli. Recently, we demonstrated an anti-apoptotic role of SGK-1 in human umbilical endothelial cells treated with high glucose. In the present study, since ceramide induces apoptosis by multiple mechanisms in diabetes and its complication such as nephropathy, we aimed to investigate whether SGK-1 may protect even against apoptosis induced by ceramide in kidney cells. Human embryonic kidney (HEK)-293 cells stable transfected with SGK-1 wild …

Cancer ResearchProgrammed cell deathCeramideSettore MED/09 - Medicina InternaDIABETES MELLITUSImmunologyProtein Serine-Threonine KinasesTNF ALPHABiologyCeramidesKidneyTransfectionImmediate-Early ProteinsSettore MED/13 - EndocrinologiaCellular and Molecular Neurosciencechemistry.chemical_compoundHumansSettore MED/49 - Scienze Tecniche Dietetiche ApplicateProtein kinase ASettore MED/04 - Patologia GeneraleSerine/threonine-specific protein kinaseTumor Necrosis Factor-alphaCERAMIDEKinaseHEK 293 cellsKidney metabolismCell BiologyLipid signalingINSULINAPOPTOSIS3. Good healthCell biologyHEK293 CellschemistryINSULIN CERAMIDE DIABETES MELLITUS TNF ALPHA APOPTOSISOriginal ArticleCell Death & Disease
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In vivo effects of tumor necrosis factor-α or flavone acetic acid in combination with doxorubicin on multidrug-resistant B16 melanoma

1996

Having observed that tumor necrosis factor (TNF)-alpha and doxorubicin (DXR) produce a synergistic inhibition of melanoma B16 and also of its multidrug resistant (MDR) variant in vitro, we tested whether this interaction would occur in vivo as well. C57BL/6 mice with s.c. tumors were treated with TNF or flavone acetic acid (FAA), a biological response modifier, in simultaneous or sequential combination with DXR. The agents were administered systemically. Overall, the results were negative, apart from a trend towards slight synergy, found in the chemosensitive melanoma, when TNF was given 1 or 2 days before DXR. The effects of FAA and DXR were found to be subadditive or antagonistic. However…

Cancer ResearchSkin NeoplasmsMelanoma ExperimentalMiceIn vivoAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsPharmacology (medical)DoxorubicinFlavonoidsPharmacologyAntibiotics AntineoplasticFlavone acetic acidDose-Response Relationship DrugTumor Necrosis Factor-alphaChemistryMelanomamedicine.diseaseDrug Resistance MultipleIn vitroMultiple drug resistanceOncologyBiochemistryDoxorubicinDrug Resistance NeoplasmCancer researchFemaleTumor necrosis factor alphaB16 melanomamedicine.drugAnti-Cancer Drugs
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Transforming growth factor-β1, β2, and β3, urokinase and parathyroid hormone-related peptide expression in 8701-BC breast cancer cells and clones

1993

8701-BC is a recently characterized cell line isolated from a primary ductal infiltrating carcinoma of the breast (d.i.c.), showing some pleomorphism in cell microanatomy at an ultrastructural level. We have obtained different sublines of 8701-BC cells by cloning in soft agar at different concentrations (0.3% and 0.6%), and we have characterized the cloned lines by some morphological and growth parameters. 8701-BC cells and clones have been submitted to analysis by reverse transcriptase-linked polymerase chain reaction to detect mRNAs of various cytokines (transforming growth factor-beta s, tumour necrosis factors, interleukin 1s, interleukin 6, parathyroid hormone-related peptide, gamma in…

Cancer Researchmedicine.medical_specialtyMolecular Sequence DataParathyroid hormoneBreast NeoplasmsPolymerase Chain ReactionTransforming Growth Factor betaInternal medicineGene expressionBiomarkers TumorTumor Cells CulturedmedicineHumansRNA MessengerMolecular BiologyBase SequencebiologyParathyroid hormone-related proteinInterleukin-6Tumor Necrosis Factor-alphaCarcinoma Ductal BreastParathyroid Hormone-Related ProteinProteinsInterleukinCell BiologyTransforming growth factor betaUrokinase-Type Plasminogen ActivatorMolecular biologyIn vitroClone CellsPhenotypeEndocrinologyCell culturebiology.proteinInterleukin-1Developmental BiologyTransforming growth factorDifferentiation
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Bcl-2 and glutathione depletion sensitizes B16 melanoma to combination therapy and eliminates metastatic disease.

2007

Abstract Purpose: Advanced melanoma resists all current therapies, and metastases in the liver are particularly problematic. Prevalent resistance factors include elevated glutathione (GSH) and increased expression of bcl-2 in melanoma cells. GSH has pleiotropic effects promoting cell growth and broad resistance to therapy, whereas Bcl-2 inhibits the activation of apoptosis and contributes to elevation of GSH. This study determined the in vivo efficacy of combination therapies administered while GSH and Bcl-2 were individually and simultaneously decreased in metastatic melanoma lesions. Experimental Design: Highly metastatic murine B16 melanoma (B16M-F10) cells have elevated levels of both G…

Cancer Researchmedicine.medical_specialtySkin NeoplasmsCombination therapyPaclitaxelGlutamineMelanoma ExperimentalBiologyMetastasischemistry.chemical_compoundMiceIn vivoInternal medicinemedicineAnimalsNeoplasm MetastasisAcivicinHematologyTumor Necrosis Factor-alphaMelanomaX-RaysGlutathioneThionucleotidesmedicine.diseaseAntineoplastic Agents PhytogenicCombined Modality TherapyGlutathioneTreatment OutcomeOncologychemistryProto-Oncogene Proteins c-bcl-2ToxicityCancer researchClinical cancer research : an official journal of the American Association for Cancer Research
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Cannabinoid CB1 receptors regulate neuronal TNF-α effects in experimental autoimmune encephalomyelitis.

2011

Abstract Cannabinoid CB1 receptors (CB1Rs) regulate the neurodegenerative damage of experimental autoimmune encephalomyelitis (EAE) and of multiple sclerosis (MS). The mechanism by which CB1R stimulation exerts protective effects is still unclear. Here we show that pharmacological activation of CB1Rs dampens the tumor necrosis factor α (TNFα)-mediated potentiation of striatal spontaneous glutamate-mediated excitatory postsynaptic currents (EPSCs), which is believed to cogently contribute to the inflammation-induced neurodegenerative damage observed in EAE mice. Furthermore, mice lacking CB1Rs showed a more severe clinical course and, in parallel, exacerbated alterations of sEPSC duration af…

Cannabinoid receptorEncephalomyelitis Autoimmune ExperimentalPolyunsaturated Alkamidesmedicine.medical_treatmentImmunologyExcitotoxicityGlutamic AcidArachidonic AcidsPharmacologyBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateReceptors Tumor Necrosis FactorAmidohydrolasesEtanerceptBehavioral Neurosciencechemistry.chemical_compoundMiceReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid Receptor ModulatorsmedicineAnimalsDronabinolReceptors AMPA6-Cyano-7-nitroquinoxaline-23-dioneMice KnockoutNeuronsEndocrine and Autonomic SystemsTumor Necrosis Factor-alphaNeurodegenerationExperimental autoimmune encephalomyelitisExcitatory Postsynaptic PotentialsAnandamidemedicine.diseaseEndocannabinoid systemCorpus StriatumMice Inbred C57BLchemistryImmunoglobulin GImmunologyNerve DegenerationSettore MED/26 - NeurologiaFemaleCannabinoidDizocilpine MaleateEndocannabinoidsBrain, behavior, and immunity
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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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1267 HSP70-2 polymorphism as a risk factor for carotid plaque rupture and cerebral ischaemia in old type 2 diabetes-atherosclerotic patients.

2005

Patients with type 2 diabetes mellitus (NIDDM) are at risk for macrovascular disease complications, such as myocardial infarction (MI) or stroke from plaque rupture. Cytokines play a key role in plaque vulnerability. IFN-gamma inhibits collagen synthesis thereby affecting plaque stability. High IL-6, TNF-alpha, and dyslipidemia are risk factors for thrombosis. Abnormal increments of HSP70 in atherosclerotic plaques might lead to plaque instability and rupture caused by chronic inflammation, which up-regulates the expression of pro-inflammatory cytokines (IL-6 and TNF-alpha) in human monocytes. Studies of a polymorphic PstI site lying in the coding region at position 1267 of the HSP70-2 gene…

Carotid Artery DiseasesMaleAgingmedicine.medical_specialtyGenotypeArteriosclerosisType 2 diabetesGastroenterologyBrain IschemiaInterferon-gammaGene FrequencyRisk FactorsInternal medicinemedicineHumansCarotid StenosisHSP70 Heat-Shock ProteinsMyocardial infarctionRNA MessengerAllelesTriglyceridesMacrovascular diseaseAgedGlycated HemoglobinRupturePolymorphism Geneticbusiness.industryInterleukin-6Tumor Necrosis Factor-alphaType 2 Diabetes MellitusOdds ratioCholesterol LDLMiddle Agedmedicine.diseaseThrombosisEndocrinologyCarotid ArteriesDiabetes Mellitus Type 2Relative riskFemalebusinessDyslipidemiaDevelopmental BiologyMechanisms of ageing and development
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Altered expression of inflammation-related genes in human carotid atherosclerotic plaques.

2011

Abstract Objective Inflammation is a pivotal process in atherosclerosis development and progression, but the underlying molecular mechanisms remain largely obscure. We have conducted an extensive expression study of atherosclerotic plaques to identify the inflammatory pathways involved in atherosclerosis. Methods We studied 11 human carotid plaques, their respective adjacent regions and 7 control arteries from different subjects. Expression of 92 genes was studied by TaqMan low-density array human inflammation panel. Human aortic endothelial and smooth muscle cells were used for in vitro experiments. Results The mRNA levels of 44/92 genes (48%) differed significantly between the tissues exa…

Carotid Artery DiseasesMalemedicine.medical_specialtyMyocytes Smooth MuscleReceptors ProstaglandinPTGS1InflammationReceptors EpoprostenolSettore MED/22 - Chirurgia VascolareMuscle Smooth VascularCytochrome P-450 Enzyme SystemInternal medicineGene expressionmedicineHumansRNA MessengerReceptors CytokineCells CulturedAgedRegulation of gene expressionInflammationbiologyTumor Necrosis Factor-alphaGene Expression ProfilingMacrophagesEndothelial CellsMiddle AgedCoculture TechniquesPlaque AtheroscleroticGene expression profilingLipoproteins LDLEndocrinologyEicosanoidEicosanoid pathwayGene Expression RegulationItalyAtherosclerosiCase-Control StudiesArachidonate 5-lipoxygenasebiology.proteinCancer researchOxidative streTumor necrosis factor alphaFemaleGene expressionmedicine.symptomInflammation MediatorsCardiology and Cardiovascular MedicineCell Adhesion MoleculesAtherosclerosis
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