Search results for "TNF"

showing 10 items of 161 documents

SAHA/TRAIL combination induces detachment and anoikis of MDA-MB231 and MCF-7 breast cancer cells

2012

Abstract SAHA, an inhibitor of histone deacetylase activity, has been shown to sensitize tumor cells to apoptosis induced by TRAIL, a member of TNF-family. In this paper we investigated the effect of SAHA/TRAIL combination in two breast cancer cell lines, the ERα−positive MCF-7 and the ERα−negative MDA-MB231. Treatment of MDA-MB231 and MCF-7 cells with SAHA in combination with TRAIL caused detachment of cells followed by anoikis, a form of apoptosis which occurs after cell detachment, while treatment with SAHA or TRAIL alone did not produce these effects. The effects were more evident in MDA-MB231 cells, which were chosen for ascertaining the mechanism of SAHA/TRAIL action. Our results show…

Recombinant Fusion ProteinsCellCASP8 and FADD-Like Apoptosis Regulating ProteinAntineoplastic AgentsBreast NeoplasmsHydroxamic AcidsCleavage (embryo)BiochemistryTNF-Related Apoptosis-Inducing LigandCell Line TumorProto-Oncogene ProteinsSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsCell AdhesionmedicineSAHA TRAIL Anoikis EGFR FAK BimELHumansAnoikisskin and connective tissue diseasesMda mb231VorinostatBcl-2-Like Protein 11ChemistryMembrane ProteinsGeneral MedicineAnoikisErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureMCF-7ApoptosisCaspasesFocal Adhesion Kinase 1ImmunologyCancer researchPhosphorylationFemaleHistone deacetylase activityApoptosis Regulatory ProteinsSignal Transduction
researchProduct

Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
researchProduct

Parthenolide sensitizes hepatocellular carcinoma cells to trail by inducing the expression of death receptors through inhibition of STAT3 activation

2011

This article shows that HepG2, Hep3B, and SK-Hep1 cells, three lines of human hepatocellular carcinoma (HCC) cells, are resistant to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Parthenolide, a sesquiterpene lactone found in European feverfew, has been shown to exert both anti-inflammatory and anti-cancer activities. This article demonstrates that co-treatment with parthenolide and TRAIL-induced apoptosis with synergistic interactions in the three lines of HCC cells. In order to explain these effects we ascertained that parthenolide increased either at protein or mRNA level the total content of death receptors TRAIL-R1 and -R2 as well as their surfac…

STAT3 Transcription FactorCarcinoma HepatocellularPhysiologyClinical BiochemistryCellDown-RegulationTRAILApoptosisPharmacologyParthenolideSTAT3TNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSettore BIO/10 - BiochimicamedicineHumansParthenolidePhosphorylationReceptorSTAT3CaspaseJanus KinasesbiologyLiver NeoplasmsProto-Oncogene Proteins c-mdm2Hep G2 CellsReceptors Death DomainCell BiologyapoptosiEnzyme ActivationGene Expression Regulation Neoplasticmedicine.anatomical_structurechemistryCell cultureApoptosisCaspasesbiology.proteinSTAT proteinDrug Screening Assays AntitumorTumor Suppressor Protein p53SesquiterpenesJournal of Cellular Physiology
researchProduct

Conjunctival Sac Fluid Contains Elevated Levels of Soluble TRAIL: Implications for the Anti-Tumoral Surveillance of the Anterior Surface of the Eye

2008

Little is known on the ability of different epithelia to release soluble TNF-related apoptosis-inducing ligand (TRAIL) and the relevance of TRAIL secretion by epithelial cells is still incompletely understood. On these bases, we have measured the concentration of soluble TRAIL by ELISA in the conjunctival sac fluid. It was the highest ever detected in a biological fluid (mean value of 26,800 pg/ml), being approximately 20-fold greater than that found in human saliva and >200-fold greater than that detected in human serum. On the other hand, osteoprotegerin, the soluble decoy receptor of TRAIL, was almost undetectable in the conjunctival sac fluid. Of note, the levels of soluble TRAIL measur…

SalivaConjunctivaPhysiologyConjunctival sac fluidClinical BiochemistryApoptosisTRAILIn Vitro TechniquesBiologySettore MED/42 - Igiene Generale E ApplicataPhotorefractive Keratectomycorneal ephiteliumFlow cytometryCorneaTNF-Related Apoptosis-Inducing LigandOsteoprotegerinCell Line TumorCorneamedicineHumansCorneal epitheliumcorneal epitheliummedicine.diagnostic_testEye NeoplasmsOsteoprotegerinEpithelial CellsCell BiologyMolecular biologyRecombinant ProteinsBody Fluidsmedicine.anatomical_structureSolubilityanti-tumoral surveillanceImmunologyConjunctival sacImmunohistochemistrytrail; conjunctival sac fluid; corneal ephitelium; anti-tumoral surveillance.Conjunctiva
researchProduct

Studies of selective TNF inhibitors in the treatment of brain injury from stroke and trauma: a review of the evidence to date

2014

Antonino Tuttolomondo, Rosaria Pecoraro, Antonio Pinto Biomedical Department of Internal and Specialistic Medicine, University of Palermo, Palermo, Italy Abstract: The brain is very actively involved in immune-inflammatory processes, and the response to several trigger factors such as trauma, hemorrhage, or ischemia causes the release of active inflammatory substances such as cytokines, which are the basis of second-level damage. During brain ischemia and after brain trauma, the intrinsic inflammatory mechanisms of the brain, as well as those of the blood, are mediated by leukocytes that communicate with each other through cytokines. A neuroinflammatory cascade has been reported to be activ…

Settore MED/09 - Medicina InternaTraumatic brain injurytumor necrosis factor inhibitorsCentral nervous systemIschemiaPharmaceutical ScienceReviewAMPA receptorEtanerceptBrain ischemiaTBIDrug DiscoverymedicineAnimalsHumansStroke trauma TNF-alfa antagonistPharmacologyMicrogliaTumor Necrosis Factor-alphabusiness.industrytraumatic brain injurylcsh:RM1-950Anti-Inflammatory Agents Non-Steroidalbrain injurymedicine.diseaseStrokelcsh:Therapeutics. Pharmacologymedicine.anatomical_structureBrain InjuriesImmunologyTumor necrosis factor alphabusinessmedicine.drugDrug Design, Development and Therapy
researchProduct

Tumor Necrosis Factor Alpha Antagonists and Occurrence of Autoantibodies in Inflammatory Bowel Disease Patients: A Single Center Experience

2015

Background & Aims: Appearance of auto antibodies have been described during anti-tumor necrosis factor (TNF) alpha therapy; however, their prevalence and clinical relevance are still unclear. We investigated prevalence of autoantibodies in inflammatory bowel diseases (IBD) patients on anti-TNFα treatment and occurrence of clinical symptoms. Methods: Titers of ANA, anti-dsDNA, SMA, AMA, LKM were evaluated from blood samples in patients receiving anti-TNFα inhibitor (adalimumab, infliximab). Results: Among 39 patients treated with anti-TNFα therapy, twenty of them developed ANA, mostly induced by infliximab. 55% ANA positive patients developed peripheral polyarthralgias with no need for inter…

Settore MED/12 - GastroenterologiaSettore MED/09 - Medicina InternaAuto antibodies TNF α Anti-tumor necrosis factor
researchProduct

Influenze della terapia con anti-TNF sulla concentrazione delle lipoproteine plasmatiche e sul rischio cardiovascolare nei pazienti affetti da Artrit…

2011

Settore MED/16 - ReumatologiaArtrite Reumatoideanti-TNFlipoproteine plasmatiche
researchProduct

No detection of hidden HBV-DNA in patients with various rheumatic diseases treated anti-TNF agents. A two-year prospective study.

2011

Settore MED/16 - Reumatologiahidden HBV-DNAanti-TNF agents.patients with various rheumatic disease
researchProduct

Genetic and clinical profile of a sicilian population with R92Q mutation

2017

Gene TNFRSF1A mutation is linked to TRAPS, autosomal dominant Autoinflammatory Disease (AID) with recurrent attacks of fever (2-3 weeks long), abdominal pain, vomiting, serositis, arthralgia and/or arthritis, myalgia, fasciitis, rash. The disease starts precociously and amyloidosis is reported in the 25% of the patients. Patients carrying the mutation R92Q usually show a mild clinical phenotype, with an extreme interindividual variability. Arthralgia and serositis are frequently less severe, however oral ulcers and pharyngitis are recurrent. Objectives: We studied the clinical and biochemical impact of the mutation R92Q in our population and the treatment outcome in all the patients with cl…

Settore MED/38 - Pediatria Generale E SpecialisticaTNFRSF1A mutation TRAPS Autoinflammatory Disease
researchProduct

TRAIL-induced apoptosis of hepatocellular carcinoma cells is augmented by targeted therapies

2009

AIM: To analyze the effect of chemotherapeutic drugs and specific kinase inhibitors, in combination with the death receptor ligand tumor necrosis factor-related apoptosis inducing ligand (TRAIL), on overcoming TRAIL resistance in hepatocellular carcinoma (HCC) and to study the efficacy of agonistic TRAIL antibodies, as well as the commitment of antiapoptotic BCL-2 proteins, in TRAIL-induced apoptosis. METHODS: Surface expression of TRAIL receptors (TRAIL-R1-4) and expression levels of the antiapoptotic BCL-2 proteins MCL-1 and BCL-xL were analyzed by flow cytometry and Western blotting, respectively. Knock-down of MCL-1 and BCL-xL was performed by transfecting specific small interfering RNA…

SorafenibCarcinoma Hepatocellularbcl-X ProteinBcl-xLAntineoplastic AgentsApoptosisTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundCell Line TumormedicineAnimalsHumansLY294002Viability assayEnzyme InhibitorsPI3K/AKT/mTOR pathwaybiologyKinaseLiver NeoplasmsGastroenterologyGeneral Medicinedigestive system diseasesReceptors TNF-Related Apoptosis-Inducing LigandchemistryProto-Oncogene Proteins c-bcl-2ApoptosisDoxorubicinCancer researchbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinTumor necrosis factor alphaOriginal ArticleFluorouracilmedicine.drug
researchProduct