Search results for "microRNA."

showing 10 items of 574 documents

Resveratrol decreases the levels of miR-155 by upregulating miR-663, a microRNA targeting JunB and JunD.

2010

An inflammatory component is present in the microenvironment of most neoplastic tissues, including those not causally related to an obvious inflammatory process. Several microRNAs, and especially miR-155, play an essential role in both the innate and adaptative immune response. Resveratrol (trans-3,4#,5-trihydroxystilbene) is a natural antioxidant with anti-inflammatory properties that is currently at the stage of preclinical studies for human cancer prevention. Here, we establish that, in human THP-1 monocytic cells as well as in human blood monocytes, resveratrol upregulates miR- 663, a microRNA potentially targeting multiple genes implicated in the immune response. In THP-1 cells, miR-66…

LipopolysaccharidesCancer ResearchJUNBProto-Oncogene Proteins c-junBlotting WesternResveratrolBiologyMonocytesmiR-15503 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemDownregulation and upregulationRNA interferencemicroRNAStilbenesBiomarkers TumorHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerLuciferases[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCells Cultured030304 developmental biologyOligonucleotide Array Sequence AnalysisCancer Biology0303 health sciencesInnate immune systemmicroRNAReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingmicroRNA; ResveratrolGeneral MedicineAntineoplastic Agents Phytogenic3. Good healthUp-RegulationTranscription Factor AP-1MicroRNAschemistryGene Expression RegulationResveratrol030220 oncology & carcinogenesisCancer research
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Transcriptomic Analyses Reveal 2 and 4 Family Members of Cytochromes P450 (CYP) Involved in LPS Inflammatory Response in Pharynx of Ciona robusta

2021

Cytochromes P450 (CYP) are enzymes responsible for the biotransformation of most endogenous and exogenous agents. The expression of each CYP is influenced by a unique combination of mechanisms and factors including genetic polymorphisms, induction by xenobiotics, and regulation by cytokines and hormones. In recent years, Ciona robusta, one of the closest living relatives of vertebrates, has become a model in various fields of biology, in particular for studying inflammatory response. Using an in vivo LPS exposure strategy, next-generation sequencing (NGS) and qRT-PCR combined with bioinformatics and in silico analyses, compared whole pharynx transcripts from naïve and LPS-exposed C. robusta…

LipopolysaccharidesLPSCytochromeQH301-705.5cytochrome P450In silicoInflammationArticleGene Expression Regulation EnzymologicCatalysisInorganic ChemistryTranscriptomeCytochrome P-450 Enzyme SystemmicroRNAmedicineAnimalsBiology (General)Physical and Theoretical ChemistryQD1-999Ciona robusta<i>Ciona robusta</i>Molecular BiologyGenePhylogenySpectroscopymiRNAInflammationGeneticschemistry.chemical_classificationbiologyGene Expression ProfilingOrganic ChemistryHigh-Throughput Nucleotide SequencingCytochrome P450General MedicineCiona intestinalisComputer Science ApplicationsChemistryEnzymechemistryMultigene FamilyNGSbiology.proteinPharynxmedicine.symptomTranscriptomeInternational Journal of Molecular Sciences
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Transcriptional regulation of miR-224 upregulated in human HCCs by NFκB inflammatory pathways

2012

Background & Aims: miR-224 is up-regulated in human HCCs as compared to both paired peri-tumoral cirrhotic tissues and cirrhotic livers without HCC. Here, we have cloned the miR-224 regulatory region and characterized its transcriptional regulation by the NFκB-dependent inflammatory pathways. Methods: Mature miRNA expression was evaluated by a 2 step stem-loop real-time RT-PCR. The recruitment of polymerase II and transcription factors on the pre-miR-224 promoter has been assessed by ChIPSeq and ChIP. Results: We found miR-224 levels strongly up-regulated in both peri-tumoral cirrhotic livers and HCC samples as compared to normal livers. In silico analysis of the putative miR-224 promoter r…

LipopolysaccharidesLiver CirrhosisMaleCarcinoma HepatocellularTranscription GeneticLiver CirrhosiLipopolysaccharideBiologyCell MovementCell Line TumormicroRNATranscriptional regulationHumansNF kappa BHCCmir-224; nfκb; hcc; mirnas; transcriptionTranscription factorLymphotoxin-alphamiRNAAgedHepatologymiRNAs; HCC; miR-224; Transcription; NF kappa BTumor Necrosis Factor-alphaLiver NeoplasmsNF-kappa BMicroRNAmiR-224HCCSMiddle AgedNFKB1Up-RegulationMicroRNAsIκBαLiverLiver NeoplasmCase-Control StudiesImmunologymiRNAsCancer researchTumor necrosis factor alphaFemaleSignal transductionCase-Control StudieTranscriptionNFκBHumanSignal Transduction
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Quaking and miR-155 interactions in inflammation and leukemogenesis.

2015

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas …

LipopolysaccharidesTime Factorsmedicine.medical_treatmentmedicine.disease_causeTransgenicMiceInnatePhosphorylationChronicB-LymphocytesLeukemiaRNA-Binding ProteinsU937 CellsLymphocyticCell biologyCytokineOncologyPhosphorylationCytokinesCLL; Glioblastoma; Inflammation; MiR-155; QKI; Animals; Apoptosis Regulatory Proteins; B-Lymphocytes; Case-Control Studies; Cytokines; Humans; Immunity Innate; Inflammation; Leukemia Lymphocytic Chronic B-Cell; Lipopolysaccharides; Macrophages; Mice; Mice Transgenic; MicroRNAs; Mitogen-Activated Protein Kinases; Phosphorylation; RAW 264.7 Cells; RNA-Binding Proteins; Signal Transduction; Time Factors; Transfection; U937 Cells; OncologySignal transductionMitogen-Activated Protein KinasesSignal Transductionp38 mitogen-activated protein kinasesOncology and CarcinogenesisMice TransgenicTransfectionNOmiR-155miR-155Downregulation and upregulationmicroRNAmedicineAnimalsHumansInflammationQKIbusiness.industryMacrophagesB-CellImmunityglioblastomaLeukemia Lymphocytic Chronic B-CellImmunity InnateMicroRNAsRAW 264.7 CellsCase-Control StudiesImmunologyCarcinogenesisbusinessApoptosis Regulatory ProteinsCLLPriority Research Paper
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Transcription factor NRF2 regulates miR-1 and miR-206 to drive tumorigenesis

2013

The mechanisms by which deregulated nuclear factor erythroid-2–related factor 2 (NRF2) and kelch-like ECH-associated protein 1 (KEAP1) signaling promote cellular proliferation and tumorigenesis are poorly understood. Using an integrated genomics and 13C-based targeted tracer fate association (TTFA) study, we found that NRF2 regulates miR-1 and miR-206 to direct carbon flux toward the pentose phosphate pathway (PPP) and the tricarboxylic acid (TCA) cycle, reprogramming glucose metabolism. Sustained activation of NRF2 signaling in cancer cells attenuated miR-1 and miR-206 expression, leading to enhanced expression of PPP genes. Conversely, overexpression of miR-1 and miR-206 decreased the exp…

Lung NeoplasmsCell SurvivalNF-E2-Related Factor 2Citric Acid CycleMice NudeBiologymedicine.disease_causeMiceRNA interferenceCarcinoma Non-Small-Cell LungCell Line TumormicroRNAGene expressionmedicineAnimalsHumansTranscription factor3' Untranslated RegionsCell ProliferationOligonucleotide Array Sequence AnalysisRegulation of gene expressionBinding SitesBase SequenceGeneral MedicineMolecular biologyHDAC4Cell biologyTumor BurdenGene Expression Regulation NeoplasticMicroRNAsCell Transformation NeoplasticGlucoseRNA InterferenceHistone deacetylaseCarcinogenesisTranscriptomeOxidation-ReductionNeoplasm TransplantationResearch Article
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Expression inactivation of SMARCA4 by microRNAs in lung tumors

2014

SMARCA4 is the catalytic subunit of the SWI/SNF chromatin-remodeling complex, which alters the interactions between DNA and histones and modifies the availability of the DNA for transcription. The latest deep sequencing of tumor genomes has reinforced the important and ubiquitous tumor suppressor role of the SWI/SNF complex in cancer. However, although SWI/SNF complex plays a key role in gene expression, the regulation of this complex itself is poorly understood. Significantly, an understanding of the regulation of SMARCA4 expression has gained in importance due to recent proposals incorporating it in therapeutic strategies that use synthetic lethal interactions between SMARCA4-MAX and SMAR…

Lung NeoplasmsDeep sequencingHistonesTranscription (biology)Catalytic DomainCell Line TumorGene expressionmicroRNAGeneticsHumansCloning MolecularMolecular BiologyTranscription factorGenetics (clinical)Cell ProliferationCell NucleusRegulation of gene expressionGeneticsbiologyDNA HelicasesHigh-Throughput Nucleotide SequencingNuclear ProteinsReproducibility of ResultsArticlesGeneral MedicineChromatin Assembly and DisassemblyPrognosisUp-RegulationCell biologyGene Expression Regulation NeoplasticMicroRNAsHistonebiology.proteinSMARCA4HeLa CellsTranscription FactorsHuman Molecular Genetics
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Genetic dissection of the miR-17∼92 cluster of microRNAs in Myc-induced B-cell lymphomas

2009

The miR-17∼92 cluster is frequently amplified or overexpressed in human cancers and has emerged as the prototypical oncogenic polycistron microRNA (miRNA). miR-17∼92 is a direct transcriptional target of c-Myc, and experiments in a mouse model of B-cell lymphomas have shown cooperation between these two oncogenes. However, both the molecular mechanism underlying this cooperation and the individual miRNAs that are responsible for it are unknown. By using a conditional knockout allele of miR-17∼92, we show here that sustained expression of endogenous miR-17∼92 is required to suppress apoptosis in Myc-driven B-cell lymphomas. Furthermore, we show that among the six miRNAs that are encoded by m…

Lymphoma B-CellGenes mycMice NudeBiologyResearch CommunicationMiceCell Line TumormicroRNAConditional gene knockoutGeneticsmedicineAnimalsAlleleGeneB cellGeneticsCancermedicine.diseaseLymphomaMice Inbred C57BLGene expression profilingMicroRNAsmedicine.anatomical_structurePerspectiveCancer researchGene DeletionDevelopmental BiologyGenes &amp; Development
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Immune pathway upregulation and lower genomic instability distinguish EBV-positive nodal T/NK-cell lymphoma from ENKTL and PTCL-NOS

2022

Primary Epstein-Barr virus (EBV)-positive nodal T/NK-cell lymphoma (PTCL-EBV) is a poorly understood disease which shows features resembling extranodal NK/T-cell lymphoma (ENKTL) and is currently not recognized as a distinct entity but categorized as a variant of primary T-cell lymphoma not otherwise specified (PTCL-NOS). Herein, we analyzed copynumber aberrations (n=77) with a focus on global measures of genomic instability and homologous recombination deficiency and performed gene expression (n=84) and EBV miRNA expression (n=24) profiling as well as targeted mutational analysis (n=16) to further characterize PTCL-EBV in relation to ENKTL and PTCL-NOS. Multivariate analysis revealed that …

Lymphoma Extranodal NK-T-CellEpstein-Barr Virus InfectionsHerpesvirus 4 HumanMicroRNAsgenomic instability EBV-positive nodal T/NK-cell lymphoma T cell lymphomahemic and lymphatic diseasesHumansLymphoma T-Cell PeripheralHematologySettore MED/08 - Anatomia PatologicaGenomic InstabilityUp-Regulation
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A role for miR-142-3p in colony-stimulating factor 1-induced monocyte differentiation into macrophages

2013

AbstractThe differentiation of human peripheral blood monocytes into macrophages can be reproduced ex vivo by culturing the cells in the presence of colony-stimulating factor 1 (CSF1). Using microarray profiling to explore the role of microRNAs (miRNAs), we identified a dramatic decrease in the expression of the hematopoietic specific miR-142-3p. Up- and down-regulation of this miRNA in primary human monocytes altered CSF1-induced differentiation of monocytes, as demonstrated by changes in the expression of the cell surface markers CD16 and CD163. One of the genes whose expression is repressed by miR-142-3p encodes the transcription factor Early Growth Response 2 (Egr2). In turn, Egr2 assoc…

Macrophage colony-stimulating factorAntigens Differentiation MyelomonocyticDown-RegulationChronic myelomonocytic leukemiaReceptors Cell SurfaceCD16BiologyGPI-Linked ProteinsMonocyte–macrophage differentiationMonocytesChronic myelomonocytic leukemiaAntigens CDCell Line TumorMiR-142-3pmedicineHumansTranscription factorMolecular BiologyEarly Growth Response Protein 2Early Growth Response Protein 1Cluster of differentiationMolecular circuitryMacrophage Colony-Stimulating FactorMacrophagesReceptors IgGCell DifferentiationLeukemia Myelomonocytic ChronicCell Biologymedicine.diseaseUp-RegulationRepressor ProteinsMicroRNAsHaematopoiesisMonocyte differentiationCancer researchEgr2K562 CellsK562 cellsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Ricerca di nuovi marcatori, diagnostici e prognostici, nella malattia di Fabry

Malattia di Fabry; microRNA; attività enzimatica; gene GLA; alfa-galattosidasi AMalattia di FabrymicroRNAgene GLAattività enzimaticaalfa-galattosidasi A
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