Search results for "silencing"

showing 10 items of 253 documents

Aurora-A Is Essential for the Tumorigenic Capacity and Chemoresistance of Colorectal Cancer Stem Cells

2010

Abstract Colorectal cancer stem cells (CR-CSC) are responsible for the generation and maintenance of intestinal tumors and are highly resistant to conventional chemotherapeutic agents. Aurora-A, a serine-threonine kinase involved in mitosis regulation, plays multiple key functions in tumor initiation and progression. We found that Aurora-A is overexpressed in primary colorectal tumor cells, in the CR-CSC fraction, and in stem cell–derived differentiated cells, compared with normal colon tissue. Aurora-A expression was functionally linked to centrosome amplification in CR-CSC, as indicated by the decrease in cells with multiple centrosomes that followed Aurora-A silencing. Knockdown of Auror…

MaleOncologyCancer Researchmedicine.medical_specialtyColorectal cancerCellular differentiationcolorectal cancer stem cellsMice NudeCell Growth ProcessesTumor initiationProtein Serine-Threonine KinasesBiologyMiceAurora KinasesCell MovementCancer stem cellInternal medicinemedicineAnimalsHumansCytotoxic T cellGene silencingMitosisAgedAurora Kinase ACentrosomeCell CycleGene AmplificationMiddle Agedmedicine.diseaseOncologyDrug Resistance NeoplasmGene Knockdown TechniquesNeoplastic Stem CellsCancer researchFemalebiological phenomena cell phenomena and immunityStem cellColorectal NeoplasmsCancer Research
researchProduct

PED is overexpressed and mediates TRAIL resistance in human non-small cell lung cancer

2008

PED (phosphoprotein enriched in diabetes) is a death-effector domain (DED) family member with a broad anti-apoptotic action. PED inhibits the assembly of the death-inducing signalling complex (DISC) of death receptors following stimulation. Recently, we reported that the expression of PED is increased in breast cancer cells and determines the refractoriness of these cells to anticancer therapy. In the present study, we focused on the role of PED in non-small cell lung cancer (NSCLC), a tumour frequently characterized by evasion of apoptosis and drug resistance. Immunohistochemical analysis of a tissue microarray, containing 160 lung cancer samples, indicated that PED was strongly expressed …

MaleProgrammed cell deathLung NeoplasmsNecrosisProtein Array AnalysisBiologyTransfectionTNF-Related Apoptosis-Inducing LigandCarcinoma Non-Small-Cell LungCell Line TumormedicineHumansGene silencingRNA Small InterferingLung cancerAgedAged 80 and overTissue microarrayAKTapoptosisIntracellular Signaling Peptides and ProteinsArticlesCell BiologyTransfectionMiddle AgedPhosphoproteinsmedicine.diseaseMolecular biologyRecombinant ProteinsUp-Regulationlung cancerReceptors TNF-Related Apoptosis-Inducing LigandDrug Resistance NeoplasmCell cultureApoptosisMolecular MedicineFemalemedicine.symptomApoptosis Regulatory ProteinsJournal of Cellular and Molecular Medicine
researchProduct

MUC1 intracellular bioactivation mediates lung fibrosis

2019

BackgroundSerum KL6/mucin 1 (MUC1) has been identified as a potential biomarker in idiopathic pulmonary fibrosis (IPF), but the role of MUC1 intracellular bioactivation in IPF is unknown.ObjectiveTo characterise MUC1 intracellular bioactivation in IPF.Methods and resultsThe expression and phosphorylation of Thr41 and Tyr46 on the intracellular MUC1-cytoplasmic tail (CT) was increased in patients with IPF (n=22) compared with healthy subjects (n=21) and localised to fibroblasts and hyperplastic alveolar type II cells. Transforming growth factor (TGF)-β1 phosphorylated SMAD3 and thereby increased the phosphorylation of MUC1-CT Thr41 and Tyr46 in lung fibroblasts and alveolar type II cells, ac…

MalePulmonary and Respiratory MedicineCellRisk AssessmentTransforming Growth Factor beta1BleomycinMice03 medical and health sciencesIdiopathic pulmonary fibrosis0302 clinical medicinemedicineAnimalsHumansGene silencingMolecular Targeted TherapyRNA MessengerSmad3 ProteinFibroblastneoplasmsCells CulturedMUC1030304 developmental biologyMice Knockout0303 health sciencesbusiness.industryBiopsy NeedleMucin-1Fibroblastsmedicine.diseaseImmunohistochemistryIdiopathic Pulmonary Fibrosisdigestive system diseasesDisease Models Animalmedicine.anatomical_structureGene Expression Regulation030228 respiratory systemCancer researchFemalebusinessMyofibroblastIntracellularSignal TransductionTransforming growth factorThorax
researchProduct

Y chromosomes: born to be destroyed

2005

Suppression of recombination is the prerequisite for stable genetically determined sex systems. A consequence of suppression of recombination is the strong bias in the distribution of transposable elements (TEs), mostly retrotransposons. Our results and those from others indicate that the major force driving the degeneration of Y chromosomes are retrotransposons in remodelling former euchromatic chromosome structures into heterochromatic ones. We put forward the following hypotheses. (1) A massive accumulation of retrotransposons occurs early in non-recombining regions. (2) Heterochromatic nucleation centres are formed as a genomic defence mechanism against invasive parasitic elements. The …

MaleRecombination GeneticTransposable elementGeneticsDosage compensationRetroelementsEuchromatinHeterochromatinGene DosageRetrotransposonSex Determination ProcessesBiologyY chromosomeGene dosageGeneral Biochemistry Genetics and Molecular BiologyEvolution MolecularHeterochromatinY ChromosomeAnimalsHumansDrosophilaFemaleGene SilencingGeneBioEssays
researchProduct

XRCC5 as a Risk Gene for Alcohol Dependence : Evidence from a Genome-Wide Gene-Set-Based Analysis and Follow-up Studies in Drosophila and Humans

2015

Genetic factors play as large a role as environmental factors in the etiology of alcohol dependence. Although genome-wide association studies (GWAS) enable systematic searches for loci not hitherto implicated in the etiology of alcohol dependence, many true findings may be missed due to correction for multiple testing. The aim of the present study was to circumvent this limitation by searching for biological system-level differences, and then following up these findings in humans and animals. Gene-set based analysis of GWAS data from 1333 cases and 2168 controls identified 19 significantly associated gene-sets of which five could be replicated in an independent sample. Clustered in these ge…

MaleRiskAdolescentMedizinGenome-wide association studyBiologyPolymorphism Single NucleotideWhite PeopleAnimals Genetically ModifiedRNA interferenceGermanyGenetic variationAnimalsHumansGene silencingGenetic Predisposition to DiseaseKu AutoantigenGeneGenetic associationPharmacologyGeneticsEthanolAlcohol dependenceDNA HelicasesCentral Nervous System DepressantsPhenotypeAlcoholismPsychiatry and Mental healthDrosophila melanogasterFemaleOriginal ArticleFollow-Up StudiesGenome-Wide Association Study
researchProduct

Downregulation of β2-microglobulin in human cord blood somatic stem cells after transplantation into livers of SCID-mice: an escape mechanism of stem…

2002

Adherently growing, non-hematopoietic somatic stem cells isolated from human cord blood were stained with the fluorescent dye PKH26 and transplanted into livers of SCID-mice to examine a possible cell fate transition. Already 7 days after transplantation stem cells were well integrated into the liver tissue. Human albumin that was not expressed by the stem cells before transplantation was detectable in the host's livers after injection of cord blood stem cells. Human alpha1-antitrypsin was detectable in stem cells already before transplantation and remained positive in the mouse liver. The most interesting observation in this study was the downregulation of human beta2-microglobulin (beta2M…

MaleTranscriptional ActivationBiophysicsDown-RegulationMice SCIDBiologyBiochemistryMiceAlbuminsAnimalsHumansGene SilencingRNA MessengerMolecular BiologyAgedStem cell transplantation for articular cartilage repairInduced stem cellsStem CellsHematopoietic Stem Cell TransplantationAmniotic stem cellsCell BiologyFetal BloodImmunohistochemistryMolecular biologyEndothelial stem cellLiverAmniotic epithelial cellsCord bloodTransplantation ToleranceStem cellbeta 2-MicroglobulinStem Cell TransplantationAdult stem cellBiochemical and Biophysical Research Communications
researchProduct

Tupaia small RNAs provide insights into function and evolution of RNAi-based transposon defense in mammals

2015

Argonaute proteins comprising Piwi-like and Argonaute-like proteins and their guiding small RNAs combat mobile DNA on the transcriptional and post-transcriptional level. While Piwi-like proteins and associated piRNAs are generally restricted to the germline, Argonaute-like proteins and siRNAs have been linked with transposon control in the germline as well as in the soma. Intriguingly, evolution has realized distinct Argonaute subfunctionalization patterns in different species but our knowledge about mammalian RNA interference pathways relies mainly on findings from the mouse model. However, mice differ from other mammals by absence of functional Piwil3 and expression of an oocyte-specific …

MaleTransposable elementendocrine systemPiwi-interacting RNAGenomic InstabilityEvolution MolecularRNA interferenceAnimalsRasiRNAGene silencingGene SilencingRNA Small InterferingMolecular BiologyMammalsTupaiaGeneticsBase Sequencebiologyurogenital systemArticlesArgonauteGerm CellsMultigene FamilyArgonaute ProteinsDNA Transposable Elementsbiology.proteinSubfunctionalizationRNA InterferenceDicerRNA
researchProduct

Epigenetic upregulation of endogenous VEGF-A reduces myocardial infarct size in mice.

2014

“Epigenetherapy” alters epigenetic status of the targeted chromatin and modifies expression of the endogenous therapeutic gene. In this study we used lentiviral in vivo delivery of small hairpin RNA (shRNA) into hearts in a murine infarction model. shRNA complementary to the promoter of vascular endothelial growth factor (VEGF-A) was able to upregulate endogenous VEGF-A expression. Histological and multiphoton microscope analysis confirmed the therapeutic effect in the transduced hearts. Magnetic resonance imaging (MRI) showed in vivo that the infarct size was significantly reduced in the treatment group 14 days after the epigenetherapy. Importantly, we show that promoter-targeted shRNA upr…

MaleVascular Endothelial Growth Factor ASmall interfering RNAAnatomy and PhysiologyTranscription GeneticMyocardial InfarctionEndogenyCardiovascularCardiovascular SystemEpigenesis GeneticSmall hairpin RNAMiceMolecular cell biologyNucleic AcidsGene expressionProtein IsoformsRNA Small InterferingCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticRegulation of gene expressionMultidisciplinaryChromosome BiologyQRGenomicsGene TherapyChromatinInterventional CardiologyCell biologyUp-RegulationVascular endothelial growth factor AMedicineEpigeneticsDNA modificationHistone modificationResearch ArticleTranscriptional ActivationDrugs and DevicesScienceDNA transcriptionBiologyDownregulation and upregulationGenomic MedicineGeneticsGene silencingAnimalsGene SilencingBiologyBase SequenceInverted Repeat Sequencesta1182Membrane ProteinsDNA MethylationPhosphoproteinsMolecular biologyMice Inbred C57BLRNAGene expressionPloS one
researchProduct

2p15-p16.1 microdeletions encompassing and proximal to BCL11A are associated with elevated HbF in addition to neurologic impairment.

2015

Elevated fetal hemoglobin (HbF) ameliorates the clinical severity of hemoglobinopathies such as β-thalassemia and sickle cell anemia. Currently, the only curative approach for individuals under chronic transfusion/chelation support therapy is allogeneic stem cell transplantation. However, recent analyses of heritable variations in HbF levels have provided a new therapeutic target for HbF reactivation: the transcriptional repressor BCL11A. Erythroid-specific BCL11A abrogation is now actively being sought as a therapeutic avenue, but the specific impact of such disruption in humans remains to be determined. Although single nucleotide polymorphisms in BCL11A erythroid regulatory elements have …

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAdolescentImmunologyBiologyBiochemistrySettore MED/38 - Pediatria Generale E SpecialisticaRed Cells Iron and ErythropoiesisInternal medicinehemic and lymphatic diseasesFetal hemoglobinmedicineGene silencingHumansChildNervous System DiseaseFetal HemoglobinNuclear ProteinHematologyNuclear ProteinsCell BiologyHematologymedicine.diseasePhenotypeSickle cell anemiaUp-RegulationTransplantationRepressor ProteinsSettore MED/03 - Genetica MedicaChromosomes Human Pair 22p15-p16.1 microdeletions BCL11A HbF neurologicImmunologyFemaleStem cellChromosome DeletionNervous System DiseasesCarrier ProteinHaploinsufficiencyCarrier ProteinsHumanBlood
researchProduct

Liver-specific methionine adenosyltransferase MAT1A gene expression is associated with a specific pattern of promoter methylation and histone acetyla…

2000

Methionine adenosyltransferase (MAT) is the enzyme that catalyzes the synthesis of S-adenosylmethionine (AdoMet), the main donor of methyl groups in the cell. In mammals MAT is the product of two genes, MAT1A and MAT2A. MAT1A is expressed only in the mature liver whereas fetal hepatocytes, extrahepatic tissues and liver cancer cells express MAT2A. The mechanisms behind the tissue and differentiation state specific MAT1A expression are not known. In the present work we examined MAT1A promoter methylation status by means of methylation sensitive restriction enzyme analysis. Our data indicate that MAT1A promoter is hypomethylated in liver and hypermethylated in kidney and fetal rat hepatocytes…

Malemedicine.drug_classBiologyBiochemistryGene Expression Regulation EnzymologicHistonesGeneticsmedicineAnimalsGene SilencingRats WistarPromoter Regions GeneticMolecular BiologyRegulation of gene expressionHistone deacetylase inhibitorNucleic Acid HybridizationAcetylationMethylationMethionine AdenosyltransferaseDNA MethylationMolecular biologyChromatinRatsHistoneLiverAcetylationHistone methyltransferaseDNA methylationCancer researchbiology.proteinBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
researchProduct