Search results for " Down-Regulation"

showing 10 items of 10 documents

HSPH1 inhibition downregulates Bcl-6 and c-Myc and hampers the growth of human aggressive B-cell non-Hodgkin lymphoma

2015

We have shown that human B-cell non-Hodgkin lymphomas (B-NHLs) express heat shock protein (HSP)H1/105 in function of their aggressiveness. Here, we now clarify its role as a functional B-NHL target by testing the hypothesis that it promotes the stabilization of key lymphoma oncoproteins. HSPH1 silencing in 4 models of aggressive B-NHLs was paralleled by Bcl-6 and c-Myc downregulation. In vitro and in vivo analysis of HSPH1-silenced Namalwa cells showed that this effect was associated with a significant growth delay and the loss of tumorigenicity when 10(4) cells were injected into mice. Interestingly, we found that HSPH1 physically interacts with c-Myc and Bcl-6 in both Namalwa cells and pr…

Lymphoma B-CellXenograft Model Antitumor AssayDNA-Binding ProteinImmunologyDown-RegulationMice SCIDSettore MED/08 - Anatomia PatologicaBiologyBiochemistryHSP110 Heat-Shock ProteinProto-Oncogene Proteins c-mycMiceDownregulation and upregulationimmune system diseasesCell Line Tumorhemic and lymphatic diseasesHeat shock proteinGene Knockdown TechniquesmedicineAnimalsHumansGene silencingHSP110 Heat-Shock ProteinsAnimals; Cell Line Tumor; DNA-Binding Proteins; Down-Regulation; Gene Knockdown Techniques; HSP110 Heat-Shock Proteins; Humans; Lymphoma B-Cell; Mice; Mice SCID; Proto-Oncogene Proteins c-myc; Xenograft Model Antitumor Assays; Biochemistry; Immunology; Medicine (all); Hematology; Cell BiologyAnimalMedicine (all)Cell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysIn vitroLymphomaDNA-Binding ProteinsCell cultureGene Knockdown TechniquesGene Knockdown TechniqueImmunologyProto-Oncogene Proteins c-bcl-6Cancer researchB-Cell Non-Hodgkin LymphomaHumanBlood
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Effects of typical inducers on olfactory xenobiotic-metabolizing enzyme, transporter, and transcription factor expression in rats.

2010

International audience; Several xenobiotic-metabolizing enzymes (XMEs) have been identified in the olfactory mucosa (OM) of mammals. However, the molecular mechanisms underlying the regulation of these enzymes have been little explored. In particular, information on the expression of the transcriptional factors in this tissue is quite limited. The aim of the present study was to examine the impact of five typical inducers, Aroclor 1254, 3-methylcholanthrene, dexamethasone, phenobarbital, and ethoxyquin, on the activities and mRNA expression of several XMEs in the OM and in the liver of rats. We also evaluated the effects of these treatments on the mRNA expression of transcription factors an…

MaleLIVERMESH : Transcription FactorsMESH: Microsomes Liver[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionPharmaceutical ScienceMESH : CytochromesMESH: Down-RegulationMESH: Membrane Transport ProteinsMESH : Down-RegulationCytosol0302 clinical medicineGlucocorticoid receptorMESH : Membrane Transport ProteinsMESH: CytosolMESH: Reverse Transcriptase Polymerase Chain ReactionGene expressionConstitutive androstane receptorMESH: Up-RegulationMESH: AnimalsReceptorMESH : Up-RegulationMESH: Cytochromes0303 health sciencesPregnane X receptorMESH : Metabolic Detoxication Phase IbiologyReverse Transcriptase Polymerase Chain ReactionMESH : RatsMESH : CytosolINDUCTIONMESH : Reverse Transcriptase Polymerase Chain ReactionMESH: Transcription FactorsUp-Regulation3. Good healthMESH : Microsomes LiverHYDROCARBON HYDROXYLASE-ACTIVITYmedicine.anatomical_structurePHASE-IBiochemistryMESH: Metabolic Detoxication Phase IIEnzyme InductionMicrosomes LiverMESH: Metabolic Detoxication Phase IMESH: XenobioticsMESH: Enzyme InductionMESH: RatsMESH : MaleDown-RegulationMESH : XenobioticsPHENOL SULFOTRANSFERASEMESH : Rats WistarXenobiotics03 medical and health sciencesOlfactory mucosaOlfactory MucosamedicineAnimalsRats WistarMESH: Olfactory MucosaTranscription factor030304 developmental biologyPharmacologyMESH : Olfactory MucosaIDENTIFICATIONRECEPTORMESH : Enzyme InductionMembrane Transport ProteinsMESH : Metabolic Detoxication Phase IIUDP-GLUCURONOSYLTRANSFERASEMESH: Rats WistarAryl hydrocarbon receptorORGANIC ANION TRANSPORTERMolecular biologyMetabolic Detoxication Phase IIMESH: MaleRatsNASAL-MUCOSAbiology.proteinCytochromesMetabolic Detoxication Phase IMESH : Animals[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryTranscription Factors
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SCD5-induced oleic acid production reduces melanoma malignancy by intracellular retention of SPARC and cathepsin B

2014

A proper balance between saturated and unsaturated fatty acids (FAs) is required for maintaining cell homeostasis. The increased demand of FAs to assemble the plasma membranes of continuously dividing cancer cells might unbalance this ratio and critically affect tumour outgrowth. We unveiled the role of the stearoyl-CoA desaturase SCD5 in converting saturated FAs into mono-unsaturated FAs during melanoma progression. SCD5 is down-regulated in advanced melanoma and its restored expression significantly reduced melanoma malignancy, both in vitro and in vivo, through a mechanism governing the secretion of extracellular matrix proteins, such as secreted protein acidic and rich in cysteine (SPAR…

cathepsin B2734Intracellular SpaceDown-RegulationCell LineMelanocyteCell Line TumormelanomaHumansintracellular acidityOsteonectinNeoplasticTumorMedicine (all)Fatty AcidsSPARCHydrogen-Ion ConcentrationGene Expression Regulation NeoplasticSCD5Gene Expression Regulationoleic acidDisease ProgressionMelanocytesFatty AcidStearoyl-CoA Desaturasecathepsin B; intracellular acidity; melanoma; oleic acid; SCD5; SPARC; Cathepsin B; Cell Line Tumor; Disease Progression; Down-Regulation; Fatty Acids; Humans; Hydrogen-Ion Concentration; Intracellular Space; Melanocytes; Melanoma; Oleic Acid; Osteonectin; Stearoyl-CoA Desaturase; Gene Expression Regulation Neoplastic; 2734; Medicine (all)Human
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Castration-Induced Downregulation of SPARC in Stromal Cells Drives Neuroendocrine Differentiation of Prostate Cancer.

2021

Abstract Fatal neuroendocrine differentiation (NED) of castration-resistant prostate cancer is a recurrent mechanism of resistance to androgen deprivation therapies (ADT) and antiandrogen receptor pathway inhibitors (ARPI) in patients. The design of effective therapies for neuroendocrine prostate cancer (NEPC) is complicated by limited knowledge of the molecular mechanisms governing NED. The paucity of acquired genomic alterations and the deregulation of epigenetic and transcription factors suggest a potential contribution from the microenvironment. In this context, whether ADT/ARPI induces stromal cells to release NED-promoting molecules and the underlying molecular networks are unestablis…

MaleCancer ResearchStromal cellAnimals Biomarkers Tumor Cell Differentiation Cell Line Tumor Coculture Techniques Endoplasmic Reticulum Chaperone BiP Epigenesis Genetic Gene Expression Regulation Neoplastic Humans Male Mice Mice Inbred C57BL Neuroendocrine Cells Osteonectin Prostatic Neoplasms Stromal Cells Transgenes Tumor Microenvironment Down-RegulationDown-RegulationContext (language use)Settore MED/08 - Anatomia PatologicaNeuroendocrine differentiationEpigenesis GeneticProstate cancerMiceStromaDownregulation and upregulationNeuroendocrine CellsCell Line TumormedicineBiomarkers TumorTumor MicroenvironmentSettore MED/05 - Patologia ClinicaAnimalsHumansOsteonectinEpigeneticsTransgenesEndoplasmic Reticulum Chaperone BiPbusiness.industryMatricellular proteinProstatic NeoplasmsCell Differentiationmedicine.diseaseCoculture TechniquesGene Expression Regulation NeoplasticMice Inbred C57BLOncologyCancer researchStromal CellsbusinessCancer research
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TpF1 from Treponema pallidum Activates Inflammasome and Promotes the Development of Regulatory T Cells

2011

Abstract Human syphilis is a multistage disease, with diverse and wide-ranging manifestations caused by Treponema pallidum. Despite the fact that a cell-mediated immune response takes part in the course of syphilis, T. pallidum often manages to evade host immunity and, in untreated individuals, may trigger chronic infection. With this study, we demonstrate for the first time, to our knowledge, that Treponema pallidum induces a regulatory T (Treg) response in patients with secondary syphilis and we found that the miniferritin TpF1, produced by the bacterium, is able to expand this response and promote the production of TGF-β. Accordingly, TpF1 stimulates monocytes to release IL-10 and TGF-β,…

AdultMaleMultiprotein complexInflammasomesVirulence FactorsCellsT-LymphocytesImmunologyAdult; Antigens Helminth; Cell Differentiation; Cells Cultured; Down-Regulation; Female; Humans; Inflammasomes; Inflammation Mediators; Male; Middle Aged; Monocytes; Syphilis; T-Lymphocytes Regulatory; Transforming Growth Factor beta; Treponema pallidum; Virulence FactorsDown-RegulationBiologyT-Lymphocytes RegulatoryMonocytesMicrobiologyProinflammatory cytokineImmune systemAntigenTransforming Growth Factor betaHelminthmedicineHumansImmunology and AllergySyphilisTreponema pallidumAntigensCells CulturedCulturedTreponemaCell DifferentiationInflammasomeMiddle Agedbiology.organism_classificationmedicine.diseaseRegulatoryChronic infectionAntigens HelminthImmunologyFemaleSyphilisInflammation Mediatorsmedicine.drugThe Journal of Immunology
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The synergistic effect of SAHA and parthenolide in MDA-MB231 breast cancer cells

2014

Abstract: The sesquiterpene lactone Parthenolide (PN) exerted a cytotoxic effect on MDA-MB231 cells, a triple-negative breast cancer (TNBC) cell line, but its effectiveness was scarce when employed at low doses. This represents an obstacle for a therapeutic utilization of PN. In order to overcome this difficulty we associated to PN the suberoylanilide hydroxamic acid (SAHA), an histone deacetylase inhibitor. Our results show that SAHA synergistically sensitized MDA-MB231 cells to the cytotoxic effect of PN. It is noteworthy that treatment with PN alone stimulated the survival pathway Akt/mTOR and the consequent nuclear translocation of Nrf2, while treatment with SAHA alone induced autophagi…

SesquiterpenePhysiologyClinical BiochemistryDown-RegulationApoptosisBreast NeoplasmsApoptosis; Autophagy; Breast Neoplasms; Cell Line Tumor; Down-Regulation; Drug Synergism; Female; Histone Deacetylase Inhibitors; Humans; Hydroxamic Acids; NF-kappa B; Sesquiterpenes; Clinical Biochemistry; Cell Biology; Physiology; Medicine (all)Hydroxamic AcidsHydroxamic AcidSettore BIO/10 - BiochimicaCell Line TumorHistone Deacetylase InhibitorAutophagyHumansBiologyVorinostatMedicine (all)NF-kappa BApoptosiDrug SynergismCell BiologyHistone Deacetylase InhibitorsFemaleHuman medicineSesquiterpenesBreast NeoplasmHumanJournal of cellular physiology
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MUC1 oncoprotein promotes refractoriness to chemotherapy in thyroid cancer cells.

2007

Abstract Overexpression of MUC1 oncoprotein is frequently observed in cancer and contributes to confer resistance to genotoxic agents. Papillary, follicular, and anaplastic thyroid carcinomas are the three forms of thyroid epithelial cancer. Anaplastic tumors are less differentiated and extremely aggressive, characterized by a poor prognosis. Little is known about the role of MUC1 in thyroid cancer. We recently showed that autocrine production of interleukin (IL)-4 and IL-10 controls thyroid cancer cell survival, growth, and resistance to chemotherapy through activation of Janus-activated kinase/signal transducers and activators of transcription (JAK/STAT) and phosphatidylinositide 3′-OH ki…

Cancer ResearchTranscription GeneticDrug ResistanceApoptosisSuppressor of Cytokine Signaling ProteinsnPhosphatidylinositol 3-KinasesAntibioticsMedicineRNA Small InterferingThyroid cancerTumorAntibiotics AntineoplasticThyroidAntineoplasticInterleukin-10Mitochondriamedicine.anatomical_structureOncologyTranscriptionSignal TransductionDown-RegulationSmall InterferingTransfectionCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinGeneticSettore MED/04 - PATOLOGIA GENERALEAntigens NeoplasmCell Line TumorHumansThyroid NeoplasmsAnaplastic thyroid cancerAntigensProtein kinase BPI3K/AKT/mTOR pathwayAntibiotics Antineoplastic; Antigens Neoplasm; Apoptosis; Cell Line Tumor; Down-Regulation; Doxorubicin; Drug Resistance Neoplasm; Humans; Interleukin-10; Interleukin-4; Mitochondria; Mucin-1; Mucins; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; RNA Small Interfering; Signal Transduction; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Transcription Genetic; Transfection; Cancer Research; Oncologybusiness.industryMucin-1MucinsCancermedicine.diseaseDoxorubicinDrug Resistance NeoplasmCancer cellCancer researchNeoplasmRNAInterleukin-4businessProto-Oncogene Proteins c-aktCancer research
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Severe reduction of blood lysosomal acid lipase activity in cryptogenic cirrhosis: A nationwide multicentre cohort study

2017

Background and aims Blood lysosomal acid lipase (LAL) is reduced in non-alcoholic steatohepatitis, which is the major cause of cryptogenic cirrhosis (CC); few data on LAL activity in CC do exist. We investigated LAL activity in a cohort of patients with liver cirrhosis. Methods This is a multicentre cohort study including 274 patients with liver cirrhosis of different aetiology from 19 centres of Internal Medicine, Gastroenterology and Hepatology distributed throughout Italy. Blood LAL activity (nmol/spot/h) was measured with dried blood spot extracts using Lalistat 2. Results Overall, 133 patients had CC, and 141 patients had cirrhosis by other causes (61 viral, 53 alcoholic, 20 alcoholic …

Liver CirrhosisMaleCryptogenic cirrhosis; Liver disease; Lysosomal acid lipase; PathogenesisCirrhosisCryptogenic cirrhosisCryptogenic cirrhosis; Liver disease; Lysosomal acid lipase; Pathogenesis; Cardiology and Cardiovascular MedicineComorbidityPathogenesisLysosonal acid lipase; non-alcoolic fatty liver disease; cirrhosis030204 cardiovascular system & hematologyGastroenterologyLiver disease0302 clinical medicineModel for End-Stage Liver DiseasePathogenesiRisk FactorsPrevalenceProspective cohort studyMultivariate AnalysiSettore MED/12 - GastroenterologiaMiddle AgedItalyCohortLinear Model030211 gastroenterology & hepatologyFemaleCardiology and Cardiovascular MedicineLiver diseaseHumanmedicine.medical_specialtyLiver CirrhosiDown-Regulation03 medical and health sciencesInternal medicineCryptogenic cirrhosis; Liver disease; Lysosomal acid lipase; Pathogenesis; Aged; Biomarkers; Chi-Square Distribution; Comorbidity; Cross-Sectional Studies; Down-Regulation; Dried Blood Spot Testing; Female; Humans; Italy; Linear Models; Liver Cirrhosis; Male; Middle Aged; Multivariate Analysis; Platelet Count; Prevalence; Risk Factors; Sterol EsterasemedicineLysosonal acid lipaseHumansnon-alcoolic fatty liver diseaseAgedCross-Sectional StudieChi-Square Distributionbusiness.industryPlatelet CountcirrhosisRisk FactorBiomarkerCholesterol ester storage diseaseHepatologySterol Esterasemedicine.diseaseCross-Sectional StudiesMultivariate AnalysisLysosomal acid lipaseLinear ModelsDried Blood Spot TestingSteatohepatitisbusinessCryptogenic cirrhosiBiomarkers
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SPARC oppositely regulates inflammation and fibrosis in bleomycin-induced lung damage.

2011

Fibrosis results from inflammatory tissue damage and impaired regeneration. In the context of bleomycin-induced pulmonary fibrosis, we demonstrated that the matricellular protein termed secreted protein acidic and rich in cysteine (SPARC) distinctly regulates inflammation and collagen deposition, depending on its cellular origin. Reciprocal Sparc(-/-) and wild-type (WT) bone marrow chimeras revealed that SPARC expression in host fibroblasts is required and sufficient to induce collagen fibrosis in a proper inflammatory environment. Accordingly, Sparc(-/-) >WT chimeras showed exacerbated inflammation and fibrosis due to the inability of Sparc(-/-) macrophages to down-regulate tumor necrosis …

Pathologymedicine.medical_specialtyAnimals; Bleomycin; Bone Marrow Cells; Chimera; Collagen; Down-Regulation; Fibroblasts; Leukocytes; Macrophages; Mice; Mice Inbred BALB C; Osteonectin; Pneumonia; Pulmonary Fibrosis; Transforming Growth Factor beta; Tumor Necrosis Factor-alphaPulmonary FibrosisDown-RegulationInflammationBone Marrow CellsBiologyPathology and Forensic MedicineMiceFibrosisTumor necrosis factor productionTransforming Growth Factor betaPulmonary fibrosismedicineLeukocytesAnimalsOsteonectinInbred BALB CChimeraTumor Necrosis Factor-alphaMacrophagesMatricellular proteinRegular ArticleSPARCTransforming growth factor betaPneumoniaFibroblastsBLEOMYCINmedicine.diseaseSPARC; BLEOMYCIN; LUNG DAMAGELUNG DAMAGECancer researchbiology.proteinTumor necrosis factor alphaCollagenmedicine.symptomOsteonectin
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The aryl hydrocarbon receptor modulates acute and late mast cell responses.

2012

Abstract The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activity is modulated by xenobiotics as well as physiological ligands. These compounds may modulate inflammatory responses and contribute to the rising prevalence of allergic diseases observed in industrialized countries. Mast cells (MCs), located within tissues at the boundary of the external environment, represent a potential target of AhR ligands. In this study, we report that murine and human MCs constitutively express AhR, and its activation by the high-affinity ligand 6-formylindolo[3,2-b]carbazole (FICZ) determines a boost in degranulation. On the contrary, repeated exposure to FICZ inhibits…

Time FactorsInbred C57BLLigandsCell DegranulationPathogenesischemistry.chemical_compoundMiceAnaphylaxiReceptorsMast CellImmunology and AllergyMast CellsReceptorMice KnockoutbiologyInterleukin-17DegranulationMast cellUp-RegulationImmunology Mast Cell Aryl Receptormedicine.anatomical_structureAryl HydrocarbonBone Marrow Celldeficiency/metabolism/physiologyIgEmedicine.symptomimmunology/metabolism/pathologyHistamineHumanReceptorTime FactorKnockoutImmunologyDown-RegulationLigandInflammationBone Marrow CellsSettore MED/08 - Anatomia PatologicaCell LinebiosynthesiAnaphylaxis; immunology/metabolism/pathology Animals Bone Marrow Cells; immunology/metabolism/pathology Cell Degranulation; genetics/immunology Cell Line Down-Regulation; genetics/immunology Humans Interleukin-17; biosynthesis Interleukin-6; biosynthesis Ligands Mast Cells; immunology/metabolism/pathology Mice Mice; Inbred C57BL Mice; Knockout Receptors; Aryl Hydrocarbon; deficiency/metabolism/physiology Receptors; IgE; physiology Time Factors Up-Regulation; genetics/immunologymedicineAnimalsHumansTranscription factorAnaphylaxisAnimalInterleukin-6Receptors IgEAryl hydrocarbon receptorgenetics/immunologyMice Inbred C57BLMAST CELL; ARYL HYDROCARBON RECEPTORchemistryReceptors Aryl HydrocarbonImmunologyphysiologybiology.proteinbiosynthesisJournal of immunology (Baltimore, Md. : 1950)
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