Search results for "gene silencing"

showing 10 items of 216 documents

Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
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PO-182 The upregulation of EPDR1 is related to tumour invasiveness in a cohort of localised colorectal cancer patients

2018

Introduction Colorectal cancer (CRC) represents a relevant public health problem. Despite new therapeutic advances, prognosis of patients diagnosed with advanced disease is still poor. The identification of new markers involved in the mechanisms of invasiveness represents a priority in order to better understand cancer development and generate new therapeutic targets. We describe here the possible role of EPDR1, a gene not yet well characterised, which encodes a protein related to ependymins, a family of piscine transmembrane proteins involved in cell adhesion. To evaluate the role of EPDR1, a translational investigation was planned to explore the consequences of the upregulation of EPDR1 i…

OncologyCancer Researchmedicine.medical_specialtyGene knockdownNecrosisCell growthColorectal cancerbusiness.industrymedicine.diseaseOncologyDownregulation and upregulationInternal medicineCohortmedicineGene silencingmedicine.symptombusinessGrading (tumors)ESMO Open
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MAD2 depletion triggers premature cellular senescence in human primary fibroblasts by activating a P53 pathway preventing aneuploid cells propagation.

2012

The spindle assembly checkpoint (SAC) is a cellular surveillance mechanism that ensures faithful chromosome segregation during mitosis and its failure can result in aneuploidy. Previously, it was suggested that reduction of the MAD2 gene, encoding a major component of the SAC, induced aneuploidy in human tumor cells. However, tumor cell lines contain multiple mutations that might affect or exacerbate the cellular response to Mad2 depletion. Thus, the scenario resulting by Mad2 depletion in primary human cells could be different and more complex that the one depicted so far. We used primary human fibroblasts (IMR90) and epithelial breast cells (MCF10A) to gain further insight on the effects …

Genome instabilityCyclin-Dependent Kinase Inhibitor p21Cell cycle checkpointMad2PhysiologyClinical BiochemistryMAD2 depletion Aneuploidy Premature cellular senescence TP53Cell Cycle ProteinsBiologyCyclin-dependent kinaseChromosome instabilityChromosomal InstabilityTumor Suppressor Protein p14ARFHumansGene SilencingRNA Small InterferingMitosisCells CulturedCellular SenescenceCell ProliferationCalcium-Binding ProteinsCell BiologyCell Cycle CheckpointsFibroblastsAneuploidybeta-GalactosidaseCell biologyRepressor ProteinsSpindle checkpointSettore BIO/18 - GeneticaGene Expression RegulationMad2 Proteinsbiology.proteinM Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Cell agingSignal Transduction
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Melatonin induces transcriptional regulation of Bim by FoxO3a in HepG2 cells

2012

Background: Melatonin induces apoptosis in many different cancer cell lines, including hepatocellular carcinoma cells. However, the responsible pathways have not been clearly elucidated. A member of the forkhead transcription factors' family, FoxO3a, has been implicated in the expression of the proapoptotic protein Bim (a Bcl-2-interacting mediator of cell death). In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate whether melatonin treatment induces Bim through regulation by the transcription factor FoxO3a. Methods: Cytotoxicity of melatonin was compared in HepG2 hepatoblastoma cells and primary human hepatocytes. Proapoptotic Bim expression was analys…

Transcriptional ActivationCancer Researchmedicine.medical_specialtyProgrammed cell deathSmall interfering RNACarcinoma HepatocellularTranscription GeneticApoptosisFoxO3amelatoninBiologyGenetics & GenomicsMelatoninDownregulation and upregulationCell Line TumorProto-Oncogene ProteinsInternal medicinemedicineTranscriptional regulationHumansGene silencingBimPhosphorylationRNA Small InterferingPromoter Regions GeneticTranscription factorBinding SitesBcl-2-Like Protein 11Forkhead Box Protein O3Membrane ProteinsForkhead Transcription FactorsHep G2 Cellshepatocellular carcinomaCell biologyEndocrinologyOncologyHepatocytesRNA Interferencebiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsChromatin immunoprecipitationProtein Bindingmedicine.drugBritish Journal of Cancer
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EphrinB2 repression through ZEB2 mediates tumour invasion and anti-angiogenic resistance.

2016

Diffuse invasion of the surrounding brain parenchyma is a major obstacle in the treatment of gliomas with various therapeutics, including anti-angiogenic agents. Here we identify the epi-/genetic and microenvironmental downregulation of ephrinB2 as a crucial step that promotes tumour invasion by abrogation of repulsive signals. We demonstrate that ephrinB2 is downregulated in human gliomas as a consequence of promoter hypermethylation and gene deletion. Consistently, genetic deletion of ephrinB2 in a murine high-grade glioma model increases invasion. Importantly, ephrinB2 gene silencing is complemented by a hypoxia-induced transcriptional repression. Mechanistically, hypoxia-inducible facto…

0301 basic medicineCell signalingScienceGeneral Physics and AstronomyRepressorDown-RegulationAngiogenesis InhibitorsEphrin-B2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleNeovascularization03 medical and health sciencesDownregulation and upregulationddc:570GliomamedicineGene silencingAnimalsHumansNeoplasm InvasivenessPsychological repressionZinc Finger E-box Binding Homeobox 2Regulation of gene expressionMice KnockoutMultidisciplinaryNeovascularization PathologicQGeneral ChemistryGliomamedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysCell HypoxiaCell biologyUp-RegulationBevacizumabGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyDrug Resistance Neoplasmmedicine.symptomNature communications
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Endoplasmic reticulum stress is involved in response of human laryngeal carcinoma cells to carboplatin but is absent in carboplatin resistant cells

2013

The major obstacle of successful tumor treatment with carboplatin (CBP) is the development of drug resistance. In the present study, we found that following treatment with CBP the amount of platinum which enters the human laryngeal carcinoma (HEp2)-derived CBP- resistant (7T) cells is reduced relative to the parental HEp2. As a consequence, the formation of reactive oxidative species (ROS) is reduced, the induction of endoplasmic reticulum (ER) stress is diminished, the amount of inter- and intrastrand cross-links is lower, and the induction of apoptosis is depressed. In HEp2 cells, ROS scavenger tempol, inhibitor of ER stress salubrinal, as well as gene silencing of ER stress marker CCAAT/…

Celllcsh:MedicineApoptosisCarboplatinSalubrinalapoptosis; carboplatin; drug resistance; endoplasmic reticulum stress; reactive oxidative species; tumor cellschemistry.chemical_compound0302 clinical medicineBlotting Southwesternlcsh:Science0303 health sciencesMultidisciplinaryThioureaGeologyEndoplasmic Reticulum Stress3. Good healthmedicine.anatomical_structure030220 oncology & carcinogenesisSignal transductionSignal TransductionResearch ArticleProgrammed cell deathCell SurvivalBlotting WesternBiologyReal-Time Polymerase Chain ReactionCyclic N-Oxides03 medical and health sciencesCell Line TumormedicineHumansGene SilencingLaryngeal NeoplasmsBiology030304 developmental biologyDNA PrimersPlatinumEndoplasmic reticulumlcsh:RCarcinomaMolecular biologychemistryCell cultureApoptosisCinnamatesDrug Resistance NeoplasmUnfolded protein responseCancer researchlcsh:QSpin LabelsReactive Oxygen Species
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Inhibition of autophagy rescues muscle atrophy in a LGMDD2 Drosophila model

2021

Limb-girdle muscular dystrophy D2 (LGMDD2) is an ultrarare autosomal dominant myopathy caused by mutation of the normal stop codon of the TNPO3 nuclear importin. The mutant protein carries a 15 amino acid C-terminal extension associated with pathogenicity. Here we report the first animal model of the disease by expressing the human mutant TNPO3 gene in Drosophila musculature or motor neurons and concomitantly silencing the endogenous expression of the fly protein ortholog. A similar genotype expressing wildtype TNPO3 served as a control. Phenotypes characterization revealed that mutant TNPO3 expression targeted at muscles or motor neurons caused LGMDD2-like phenotypes such as muscle degener…

MaleMutantBiochemistryAnimals Genetically ModifiedMutant proteinAutophagyGeneticsmedicineAnimalsHumansGene silencingMuscular dystrophyMyopathyMolecular BiologyMotor NeuronsbiologyMusclesAutophagyChloroquinebeta Karyopherinsmedicine.diseasebiology.organism_classificationMuscle atrophyCell biologySurvival RateDisease Models AnimalMuscular AtrophyDrosophila melanogasterPhenotypeMuscular Dystrophies Limb-GirdleInsect HormonesFemalemedicine.symptomDrosophila melanogasterLocomotionBiotechnologyThe FASEB Journal
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Protease-mediated processing of Argonaute proteins controls small RNA association

2020

SummarySmall RNA pathways defend the germlines of animals against selfish genetic elements and help to maintain genomic integrity. At the same time, their activity needs to be well-controlled to prevent silencing of ‘self’ genes. Here, we reveal a proteolytic mechanism that controls endogenous small interfering (22G) RNA activity in the Caenorhabditis elegans germline to protect genome integrity and maintain fertility. We find that WAGO-1 and WAGO-3 Argonaute (Ago) proteins are matured through proteolytic processing of their unusually proline-rich N-termini. In the absence of DPF-3, a P-granule-localized N-terminal dipeptidase orthologous to mammalian DPP8/9, processing fails, causing a cha…

Transposable elementSmall RNAanimal structuresDNA damageBiologyDipeptidyl peptidaseSubstrate Specificity03 medical and health sciences0302 clinical medicineAnimalsGene silencingRNA MessengerRNA Small InterferingCaenorhabditis elegansCaenorhabditis elegans ProteinsDipeptidyl-Peptidases and Tripeptidyl-PeptidasesMolecular BiologyGeneCaenorhabditis elegans030304 developmental biology0303 health sciencesWild typeRNACell BiologyArgonautebiology.organism_classificationCell biologyFertilityArgonaute ProteinsProteolysisRNA HelminthProtein Processing Post-Translational030217 neurology & neurosurgery
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Epigenetic Silencing of CDR1as Drives IGF2BP3-Mediated Melanoma Invasion and Metastasis.

2018

Summary Metastasis is the primary cause of death of cancer patients. Dissecting mechanisms governing metastatic spread may uncover important tumor biology and/or yield promising therapeutic insights. Here, we investigated the role of circular RNAs (circRNA) in metastasis, using melanoma as a model aggressive tumor. We identified silencing of cerebellar degeneration-related 1 antisense (CDR1as), a regulator of miR-7, as a hallmark of melanoma progression. CDR1as depletion results from epigenetic silencing of LINC00632, its originating long non-coding RNA (lncRNA) and promotes invasion in vitro and metastasis in vivo through a miR-7-independent, IGF2BP3-mediated mechanism. Moreover, CDR1as le…

0301 basic medicineCancer ResearchRegulatorNerve Tissue ProteinsBiologyAutoantigensArticleMetastasisEpigenesis Genetic03 medical and health sciences0302 clinical medicinemedicineGene silencingHumansEnhancer of Zeste Homolog 2 ProteinNeoplasm InvasivenessRNA AntisenseGene SilencingNeoplasm MetastasisMelanomaMelanomaEZH2RNACancerRNA-Binding ProteinsRNA Circularmedicine.diseasePhospholipid Hydroperoxide Glutathione PeroxidasePrognosisMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchbiology.proteinRNA Long NoncodingPRC2Cancer cell
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Development of a simple, biocompatible and cost-effective Inulin-Diethylenetriamine based siRNA delivery system

2015

Small interfering RNAs (siRNAs) have the potential to be of therapeutic value for many human diseases. So far, however, a serious obstacle to their therapeutic use is represented by the absence of appropriate delivery systems able to protect them from degradation and to allow an efficient cellular uptake. In this work we developed a siRNA delivery system based on inulin (Inu), an abundant and natural polysaccharide. Inu was functionalized via the conjugation with diethylenetriamine (DETA) residues to form the complex Inu-DETA. We studied the size, surface charge and the shape of the Inu-DETA/siRNA complexes; additionally, the cytotoxicity, the silencing efficacy and the cell uptake-mechanis…

3003Small interfering RNAJHH6CellPharmaceutical ScienceEndocytosisCell LineIn vivoCell Line TumormedicinePolyaminesGene silencingHumansMicropinocytosisRNA Small InterferingCytotoxicityChemistry16HBEInulinEndocytosisDiethylenetriamine (DETA)Cell biologyInu-DETA copolymermedicine.anatomical_structureBiochemistryCytoplasmSettore CHIM/09 - Farmaceutico Tecnologico ApplicativosiRNA16HBE; Diethylenetriamine (DETA); Inu-DETA copolymer; Inulin; JHH6; siRNA; 3003E2F1 Transcription Factor
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