Search results for " Gene Expression Regulation"

showing 10 items of 70 documents

Aging-associated genes and let-7 microRNAs: a contribution to myogenic program dysregulation in oculopharyngeal muscular dystrophy

2019

Oculopharyngeal muscular dystrophy (OPMD) is a late-onset muscle disease caused by an abnormal (GCN) triplet expansion within the polyadenylate-binding protein nuclear 1 gene and consequent mRNA pr...

0301 basic medicineMaleAgingOculopharyngealMuscle DevelopmentBiochemistryMyoblasts0302 clinical medicine80 and overMuscular DystrophyHMGB1 ProteinPAX7 Transcription FactorCell DifferentiationdifferentiationMiddle AgedCell biologymedicine.anatomical_structureFemaleMyogeninMitogen-Activated Protein KinasesBiotechnologyDifferentiation regeneration skeletal muscleAdultBiologyInclusion BodyOculopharyngeal muscular dystrophy03 medical and health sciencesmicroRNAGeneticsmedicineHumansGenetic Predisposition to Diseasedifferentiation; regeneration; skeletal muscle; Adult; Aged; Aged 80 and over; Aging; Antigens Neoplasm; Cell Differentiation; Female; Gene Expression Regulation; HMGB1 Protein; Humans; Male; MicroRNAs; Middle Aged; Mitogen-Activated Protein Kinases; Muscle Development; Muscular Dystrophy Oculopharyngeal; Myoblasts; Myogenin; Myositis Inclusion Body; PAX7 Transcription Factor; Genetic Predisposition to Diseaseskeletal muscleAntigensMolecular BiologyGeneAgedMessenger RNAMyositisRegeneration (biology)Skeletal musclemedicine.diseaseMicroRNAs030104 developmental biologyMuscle diseaseGene Expression RegulationregenerationNeoplasm030217 neurology & neurosurgery
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Influence of middle-distance running on muscular micro RNAs

2018

A specific subset of micro RNAs (miRs), including miR-133 and miR-206, is specifically expressed in muscle tissue, so that they are currently defined as muscular miRs (myomiRs). To further elucidate the role of myomiRs in muscle biology, we measured miR-133a and miR-206 in plasma of 28 middle-age recreational athletes. The study population consisted of 28 middle aged, recreation athletes (11 women and 17 men; mean age, 46 years) who completed a 21.1 km, half-marathon. The plasma concentration of miR-133a and miR-206, the serum concentration of creatine kinase (CK) and high-sensitivity (HS) cardiac troponin T (cTnT), as well as capillary lactate, were measured before and immediately after th…

0301 basic medicineMuscle tissueMalemedicine.medical_specialtyClinical BiochemistryRunning03 medical and health sciencesTroponin complexDistance runningTroponin TInternal medicinemedicineHumansLactic AcidMuscle SkeletalCreatine KinasemiRNAProlonged exercisebiologyepigeneticsexercisemicroRNAepigenetics; exercise; microRNA; miRNA; Running; sport; Athletes; Creatine Kinase; Female; Gene Expression Regulation; Humans; Lactic Acid; Male; MicroRNAs; Middle Aged; Multivariate Analysis; Muscle Skeletal; Physical Endurance; Running; Troponin TGeneral MedicineSkeletalrunning; epigenetics; exercise; miRNA; microRNA; sportMiddle AgedRunning timeMicroRNAs030104 developmental biologyEndocrinologymedicine.anatomical_structureGene Expression RegulationBiological significanceAthletesMultivariate Analysisbiology.proteinPhysical EndurancePopulation studyMuscleCreatine kinaseFemalesport
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Epigenomic landscape of human colorectal cancer unveils an aberrant core of pan-cancer enhancers orchestrated by YAP/TAZ

2021

Cancer is characterized by pervasive epigenetic alterations with enhancer dysfunction orchestrating the aberrant cancer transcriptional programs and transcriptional dependencies. Here, we epigenetically characterize human colorectal cancer (CRC) using de novo chromatin state discovery on a library of different patient-derived organoids. By exploring this resource, we unveil a tumor-specific deregulated enhancerome that is cancer cell-intrinsic and independent of interpatient heterogeneity. We show that the transcriptional coactivators YAP/TAZ act as key regulators of the conserved CRC gained enhancers. The same YAP/TAZ-bound enhancers display active chromatin profiles across diverse human t…

0301 basic medicineOrganoidEpigenomicsTranscription FactorGeneral Physics and AstronomyColorectal NeoplasmAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Tumor Cells Cultured; Enhancer Elements Genetic; Epigenesis GeneticEpigenesis Genetic0302 clinical medicineModelsAdaptor Proteins Signal Transducing Colorectal Neoplasms Gene Expression Regulation NeoplasticHistone Code Humans Models Genetic Organoids RNA-Seq Single-Cell Analysis Trans-Activators Transcription Factors Tumor Cells Cultured Enhancer Elements Genetic Epigenesis GeneticTumor Cells CulturedCancer genomicsHistone codeRNA-SeqEpigenomicsAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Transcriptional Coactivator with PDZ-Binding Motif Proteins; Tumor Cells Cultured; YAP-Signaling Proteins; Enhancer Elements Genetic; Epigenesis GeneticMultidisciplinaryCulturedQAdaptor Proteins3. Good healthChromatinTumor CellsGene Expression Regulation NeoplasticHistone CodeOrganoidsSingle-Cell AnalysiEnhancer Elements GeneticTrans-Activator030220 oncology & carcinogenesisSingle-Cell AnalysisColorectal NeoplasmsHumanEnhancer ElementsScienceTumour heterogeneityBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesGeneticmedicineHumansEpigeneticsEnhancerTranscription factorAdaptor Proteins Signal TransducingNeoplasticModels GeneticSignal TransducingCancerYAP-Signaling ProteinsGeneral Chemistrymedicine.diseaseColorectal cancerdigestive system diseases030104 developmental biologyGene Expression RegulationTranscriptional Coactivator with PDZ-Binding Motif ProteinsCancer cellCancer researchTrans-ActivatorsEpigenesisTranscription Factors
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Chemoresistance and chemosensitization in cholangiocarcinoma

2017

One of the main difficulties in the management of patients with advanced cholangiocarcinoma (CCA) is their poor response to available chemotherapy. This is the result of powerful mechanisms of chemoresistance (MOC) of quite diverse nature that usually act synergistically. The problem is often worsened by altered MOC gene expression in response to pharmacological treatment. Since CCA includes a heterogeneous group of cancers their genetic signature coding for MOC genes is also diverse; however, several shared traits have been defined. Some of these characteristics are shared with other types of liver cancer, namely hepatocellular carcinoma and hepatoblastoma. An important goal in modern onco…

0301 basic medicinePharmacologybile ductschemotherapydrug delivery systems0302 clinical medicineChemosensitizationantineoplastic agentsmolecular biologyReceptorhumansreceptor protein-tyrosine kinasesmedia_commonapoptosisgene expression regulationbile duct neoplasmsDrug Resistance Multipletargeted therapiesGene Expression Regulation Neoplasticmultiplebiliary cancer; chemotherapy; liver cancer; multidrug resistance; targeted therapies; antineoplastic agents; apoptosis; bile duct neoplasms; bile ducts; cell survival; cholangiocarcinoma; drug delivery systems; drug resistance multiple; drug resistance; neoplasm; epithelial cells; gene expression regulation neoplastic; genetic therapy; humans; protein kinase inhibitors; receptor protein-tyrosine kinases; signal transduction; treatment outcome; molecular medicine; molecular biology030220 oncology & carcinogenesisHepatocellular carcinomabiliary cancerLiver cancercholangiocarcinomaTyrosine kinasesignal transductionDrugHepatoblastomamedia_common.quotation_subjectcell survivalPharmacological treatmentliver cancer03 medical and health sciencesmultidrug resistancemedicinemolecular medicinedrug resistancebusiness.industrymedicine.diseaseepithelial cellsneoplasticprotein kinase inhibitors030104 developmental biologyDrug Resistance NeoplasmCancer researchtreatment outcomebusinessneoplasmgenetic therapy
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Insulin Dissociates the Effects of Liver X Receptor on Lipogenesis, Endoplasmic Reticulum Stress, and Inflammation

2016

IF 4.258; International audience; Diabetes is characterized by increased lipogenesis as well as increased endoplasmic reticulum (ER) stress and inflammation. The nuclear hormone receptor liver X receptor (LXR) is induced by insulin and is a key regulator of lipid metabolism. It promotes lipogenesis and cholesterol efflux, but suppresses endoplasmic reticulum stress and inflammation. The goal of these studies was to dissect the effects of insulin on LXR action. We used antisense oligonucleotides to knock down Lxr alpha in mice with hepatocytespecific deletion of the insulin receptor and their controls. We found, surprisingly, that knock-out of the insulin receptor and knockdown of Lxr alpha …

0301 basic medicinemedicine.medical_treatmentLipid-metabolismResistanceBiochemistryHepatitisMESH: HepatitisMESH: Endoplasmic Reticulum Stresspolycyclic compoundsInsulinGene-expressionPhospholipidsLiver X ReceptorsMice KnockoutbiologyMESH : Gene Expression RegulationFatty-acid synthesisfood and beveragesEndoplasmic Reticulum StressOrphan Nuclear ReceptorsCultured-cellsLipidsMESH: Gene Expression RegulationMESH : Endoplasmic Reticulum StressMessenger-rnaLiverMESH: Orphan Nuclear ReceptorsGene Knockdown TechniquesLipogenesisFemalelipids (amino acids peptides and proteins)Signal Transductionliver X receptormedicine.medical_specialtyLxr-alphaMice Transgenicdigestive systemPhospholipid transfer proteinGene Expression Regulation Enzymologic03 medical and health sciencesInsulin resistanceMESH : HepatitisLysophosphatidylcholine acyltransferaseInternal medicinemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyLiver X receptorMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCrosses GeneticLipogenesisEndoplasmic reticulumInsulinElement-binding protein-1cMESH : LiverCell Biologymedicine.diseaseMESH : Orphan Nuclear ReceptorsReceptor InsulinMice Inbred C57BLInsulin receptor030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2Gene Expression RegulationNuclear receptorbiology.proteinUnfolded protein responseInsulin ResistanceMESH: Liver
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Cytotoxicity of cucurbitacin E from Citrullus colocynthis against multidrug-resistant cancer cells

2019

Abstract Background Cucurbitacin E (CuE) is an oxygenated tetracyclic triterpenoid isolated from the fruits of Citrullus colocynthis (L.) Schrad. Purpose This study outlines CuE's cytotoxic activity against drug-resistant tumor cell lines. Three members of ABC transporters superfamily, P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and ABCB5 were investigated, whose overexpression in tumors is tightly linked to multidrug resistance. Further factors of drug resistance studied were the tumor suppressor TP53 and the epidermal growth factor receptor (EGFR). Methods Cytotoxicity assays (resazurin assays) were used to investigate the activity of Citrullus colocynthis and CuE towar…

Abcg2Drug ResistancePharmaceutical ScienceATP-binding cassette transporterMicroarraySubfamily Gchemistry.chemical_compoundGene Knockout Techniques0302 clinical medicineEpidermal growth factorPhytogenicDrug DiscoveryATP Binding Cassette Transporter Subfamily G Member 2Cancer0303 health sciencesTumorLeukemiabiologyChemistryABCB5TransfectionCell cycleNeoplasm ProteinsGene Expression Regulation NeoplasticErbB ReceptorsMolecular Docking SimulationSubfamily B030220 oncology & carcinogenesisMolecular MedicineCitrullus colocynthiMember 2Member 1ATP Binding Cassette Transporter Subfamily BATP Binding Cassette TransporterAntineoplastic AgentsCell Line03 medical and health sciencesCell Line TumorHumansATP Binding Cassette Transporter Subfamily B Member 1030304 developmental biologyCucurbitacin EPharmacologyNeoplasticTraditional herbal medicineCancer; Citrullus colocynthis; Drug resistance; Microarray; Traditional herbal medicine; ATP Binding Cassette Transporter Subfamily B; ATP Binding Cassette Transporter Subfamily B Member 1; ATP Binding Cassette Transporter Subfamily G Member 2; Antineoplastic Agents Phytogenic; Cell Line Tumor; Citrullus colocynthis; Doxorubicin; Drug Resistance Neoplasm; ErbB Receptors; Gene Expression Regulation Neoplastic; Gene Knockout Techniques; Humans; Leukemia; Molecular Docking Simulation; Neoplasm Proteins; Triterpenes; Tumor Suppressor Protein p53Antineoplastic Agents PhytogenicTriterpenesComplementary and alternative medicineGene Expression RegulationDrug Resistance NeoplasmDoxorubicinCancer cellbiology.proteinCancer researchNeoplasmCitrullus colocynthisTumor Suppressor Protein p53
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Stat3 and Gfi-1 Transcription Factors Control Th17 Cell Immunosuppressive Activity via the Regulation of Ectonucleotidase Expression

2012

International audience; Although Th17 cells are known to promote tissue inflammation and autoimmunity, their role during cancer progression remains elusive. Here, we showed that in vitro Th17 cells generated with the cytokines IL-6 and TGF-β expressed CD39 and CD73 ectonucleotidases, leading to adenosine release and the subsequent suppression of CD4(+) and CD8(+) T cell effector functions. The IL-6-mediated activation of the transcription factor Stat3 and the TGF-β-driven downregulation of Gfi-1 transcription factor were both essential for the expression of ectonucleotidases during Th17 cell differentiation. Stat3 supported whereas Gfi-1 repressed CD39 and CD73 expression by binding to thei…

Adoptive cell transferMESH : Transcription FactorsCellular differentiationMESH: Th17 CellsT-LymphocytesCellMESH : Promoter Regions GeneticMESH : RNA Small InterferingMESH: Mice KnockoutMice0302 clinical medicineTransforming Growth Factor betaMESH: RNA Small InterferingMESH : STAT3 Transcription FactorImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyEctonucleotidaseMESH: AnimalsRNA Small InterferingSTAT3MESH: Lymphocytes Tumor-InfiltratingPromoter Regions GeneticMESH: Antigens CD5'-NucleotidaseRegulation of gene expressionMice Knockout0303 health sciencesMESH : Gene Expression RegulationApyraseMESH: STAT3 Transcription FactorMESH: Transcription FactorsMESH: Gene Expression RegulationMESH : Mice TransgenicCell biologyMESH : Lymphocytes Tumor-InfiltratingDNA-Binding ProteinsMESH : ApyraseInfectious Diseasesmedicine.anatomical_structure[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : DNA-Binding ProteinsMESH: ApyraseSTAT3 Transcription Factor[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Interleukin-6MESH: Mice TransgenicT cellImmunologyMice TransgenicMESH : Mice Inbred C57BLBiology03 medical and health sciencesLymphocytes Tumor-InfiltratingMESH: Mice Inbred C57BLAntigens CDMESH: Promoter Regions GeneticMESH : 5'-NucleotidaseMESH : MicemedicineMESH : Antigens CDMESH : Th17 CellsAnimalsTranscription factorMESH: MiceMESH: Transforming Growth Factor beta030304 developmental biologyMESH : T-LymphocytesBinding SitesInterleukin-6MESH: Interleukin-6Mice Inbred C57BLMESH: T-LymphocytesMESH : Transforming Growth Factor betaMESH: Binding SitesGene Expression Regulationbiology.proteinMESH : Mice KnockoutTh17 CellsMESH : AnimalsMESH: 5'-NucleotidaseMESH: DNA-Binding ProteinsMESH : Binding Sites030215 immunologyTranscription FactorsImmunity
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The transcription factor IFN regulatory factor–4 controls experimental colitis in mice via T cell–derived IL-6

2008

The proinflammatory cytokine IL-6 seems to have an important role in the intestinal inflammation that characterizes inflammatory bowel diseases (IBDs) such as Crohn disease and ulcerative colitis. However, little is known about the molecular mechanisms regulating IL-6 production in IBD. Here, we assessed the role of the transcriptional regulator IFN regulatory factor-4 (IRF4) in this process. Patients with either Crohn disease or ulcerative colitis exhibited increased IRF4 expression in lamina propria CD3+ T cells as compared with control patients. Consistent with IRF4 having a regulatory function in T cells, in a mouse model of IBD whereby colitis is induced in RAG-deficient mice by transp…

AdultCD4-Positive T-LymphocytesMaleAdoptive cell transferRecombinant Fusion ProteinsT-LymphocytesCD3T cellAdoptive Transfer; Adult; Animals; Apoptosis; CD4-Positive T-Lymphocytes; Colitis; Cytokines; DNA-Binding Proteins; Female; Gene Expression Regulation; Humans; Inflammatory Bowel Diseases; Interferon Regulatory Factors; Interleukin-6; Intestinal Mucosa; Male; Mice; Mice Inbred C57BL; Mice Knockout; Middle Aged; Oxazolone; Receptors Interleukin-6; Recombinant Fusion Proteins; T-Lymphocytes; Trinitrobenzenesulfonic AcidApoptosisProinflammatory cytokineMiceIntestinal mucosamedicineAnimalsHumansIntestinal MucosaColitisInterleukin 6Mice KnockoutbiologyInterleukin-6OxazoloneGeneral MedicineMiddle AgedColitisInflammatory Bowel Diseasesmedicine.diseaseAdoptive TransferReceptors Interleukin-6Ulcerative colitisDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationTrinitrobenzenesulfonic AcidInterferon Regulatory FactorsImmunologybiology.proteinCytokinesFemaleResearch ArticleJournal of Clinical Investigation
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Prognostic significance of miR-34a in Ewing sarcoma is associated with cyclin D1 and ki-67 expression.

2014

ABSTRACT Background At diagnosis, identification of reliable biological indicators of prognosis to allow stratification of patients according to different risks is an important but still unresolved aspect in the treatment of Ewing sarcoma (EWS) patients. This study aimed to explore the role of miR-34A expression on prognosis of EWS patients. Patients and methods Specimens from 109 patients with non-metastatic EWS treated at the Rizzoli Institute with neoadjuvant chemotherapy (protocols ISG/SSGIII, EW-1, EW-2, EW-REN2, EW-REN3, EW-PILOT) and 17 metastases were studied. Sixty-eight patients (62%) remained disease-free and 41 (38%) relapsed (median follow-up: 67 months, range 9–241 months). Ex…

AdultMalePrognosiHydro-Lyasemedicine.medical_treatmentSarcoma EwingDisease-Free SurvivalCyclin D1medicineHumansCyclin D1Neoplasm Metastasisprognostic biomarkerNeoadjuvant therapyHydro-LyasesAged 80 and overTissue microarraybiologybusiness.industryProportional hazards modelMedicine (all)Ewing's sarcomaMicroRNAHematologyMiddle Agedmedicine.diseasePrognosisNeoadjuvant TherapyNeoplasm MetastasiGene Expression Regulation NeoplasticMicroRNAsKi-67 AntigenTreatment OutcomeOncologyDrug Resistance NeoplasmKi-67biology.proteinCancer researchKi-67ImmunohistochemistryFemaleSarcomacyclin D1; Ewing sarcoma; Ki-67; miR-34a; prognostic biomarkers; Adult; Aged 80 and over; Cyclin D1; Disease-Free Survival; Drug Resistance Neoplasm; Female; Gene Expression Regulation Neoplastic; Humans; Hydro-Lyases; Ki-67 Antigen; Male; MicroRNAs; Middle Aged; Neoadjuvant Therapy; Neoplasm Metastasis; Prognosis; Sarcoma Ewing; Treatment Outcome; Medicine (all)businessEwing sarcomamiR-34aHumanAnnals of oncology : official journal of the European Society for Medical Oncology
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Glycogen synthase 2 is a novel target gene of peroxisome proliferator-activated receptors.

2007

International audience; Glycogen synthase 2 (Gys-2) is the ratelimiting enzyme in the storage of glycogen in liver and adipose tissue, yet little is known about regulation of Gys-2 transcription. The peroxisome proliferator-activated receptors (PPARs) are transcription factors involved in the regulation of lipid and glucose metabolism and might be hypothesized to govern glycogen synthesis as well. Here, we show that Gys-2 is a direct target gene of PPARalpha, PPARbeta/delta and PPARgamma. Expression of Gys-2 is significantly reduced in adipose tissue of PPARalpha-/-, PPARbeta/delta-/- and PPARgamma+/- mice. Furthermore, synthetic PPARbeta/delta, and gamma agonists markedly up-regulate Gys-2…

Animals; Chromatin/ultrastructure; DNA Primers; Gene Expression Regulation Enzymologic; Glycogen Synthase/genetics; Hepatocytes/enzymology; Hepatocytes/physiology; Mice; Mice Knockout; Peroxisome Proliferator-Activated Receptors/deficiency; Peroxisome Proliferator-Activated Receptors/genetics; Polymerase Chain Reaction; RNA/genetics; RNA/isolation & purification; Rats; Transcription GeneticTranscription GeneticPeroxisome proliferator-activated receptorMESH : HepatocytesPPREPolymerase Chain Reactionadipose-tissuePPARMESH: HepatocytesMice0302 clinical medicineMESH: Animals610 Medicine & healthchemistry.chemical_classificationRegulation of gene expression0303 health sciencesGlycogenglycogen-synthaseChromatinGlycogen Synthase030220 oncology & carcinogenesisMESH : DNA PrimersmicroarrayMESH: DNA Primersmedicine.medical_specialtyHealth aging / healthy living [IGMD 5]fatty-acid oxidationliverGene Expression Regulation EnzymologicMESH: Chromatin03 medical and health sciencesskeletal-muscleGlycogen synthaseMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyHNF4αVLAGPharmacologybeta/deltaMESH: Polymerase Chain Reactionresponse elementsMESH : Peroxisome Proliferator-Activated ReceptorsEndocrinologychemistryMicrobial pathogenesis and host defense [UMCN 4.1]Response elementPeroxisome Proliferator-Activated ReceptorsAdipose tissueMESH: Peroxisome Proliferator-Activated Receptorsin-vivoMESH: Mice KnockoutTransactivationchemistry.chemical_compoundVoeding Metabolisme en GenomicaMESH : RNAMESH : Polymerase Chain ReactionMice KnockoutMESH : ChromatinMESH : RatsMESH: Gene Expression Regulation EnzymologicMetabolism and Genomicsadipose tissueMetabolisme en GenomicaMolecular MedicineNutrition Metabolism and GenomicsMESH : Glycogen SynthaseResearch ArticleMESH: Ratsglycogen synthase 2610 Medicine & healthBiologyMESH : Gene Expression Regulation EnzymologicCellular and Molecular NeuroscienceVoedingMESH: RNAInternal medicineMESH : MicemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyTranscription factorMESH: Micealpha ppar-alpha030304 developmental biologyNutritionDNA PrimersMESH: Glycogen SynthaseMESH: Transcription GeneticMESH : Transcription GeneticCell BiologyRatsgene transcriptionbiology.proteinHepatocytesRNAMESH : Mice KnockoutgammaMESH : Animalsmetabolism
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