Search results for "Oligonucleotides"

showing 10 items of 95 documents

MiR-205-5p inhibition by locked nucleic acids impairs metastatic potential of breast cancer cells.

2018

AbstractMir-205 plays an important role in epithelial biogenesis and in mammary gland development but its role in cancer still remains controversial depending on the specific cellular context and target genes. We have previously reported that miR-205-5p is upregulated in breast cancer stem cells targeting ERBB pathway and leading to targeted therapy resistance. Here we show that miR-205-5p regulates tumorigenic properties of breast cancer cells, as well as epithelial to mesenchymal transition. Silencing this miRNA in breast cancer results in reduced tumor growth and metastatic spreading in mouse models. Moreover, we show that miR-205-5p knock-down can be obtained with the use of specific lo…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal Transitionmedicine.medical_treatmentAntagomirSettore MED/50 - Scienze Tecniche Mediche ApplicateImmunologyTransplantation HeterologousOligonucleotidesBreast NeoplasmsBiologyArticleTargeted therapy03 medical and health sciencesCellular and Molecular NeuroscienceMiceBreast cancerErbBCell MovementMice Inbred NODOligonucleotideCell Line TumormicroRNAmedicineGene silencingAnimalsHumansEpithelial–mesenchymal transitionlcsh:QH573-671Neoplasm MetastasisCell ProliferationAnimallcsh:CytologyCancerAntagomirsMicroRNACell Biologymedicine.diseaseNeoplasm MetastasiMicroRNAs030104 developmental biologyCancer researchFemaleStem cellBreast NeoplasmHumanCell deathdisease
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The future of Extracellular Vesicles as Theranostics – an ISEV meeting report

2020

ABSTRACT The utilization of extracellular vesicles (EVs) in clinical theranostics has rapidly advanced in the past decade. In November 2018, the International Society for Extracellular Vesicles (ISEV) held a workshop on “EVs in Clinical Theranostic”. Here, we report the conclusions of roundtable discussions on the current advancement in the analysis technologies and we provide some guidelines to researchers in the field to consider the use of EVs in clinical application. The main challenges and the requirements for EV separation and characterization strategies, quality control and clinical investigation were discussed to promote the application of EVs in future clinical studies.

0301 basic medicineEngineeringHistologytheranosticMeeting ReportFreeze thawingExtracellular vesiclesCa 19 9 antigen03 medical and health sciences0302 clinical medicineClinical investigationIn vitro studylcsh:QH573-671therapylcsh:Cytologybusiness.industryDietary intakeAntibody affinityCell BiologyExtracellular vesicles030104 developmental biology030220 oncology & carcinogenesisAntisense oligonucleotidesbiomarkerEngineering ethicsbusinessJournal of Extracellular Vesicles
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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Inhibition of STAT3 with the generation 2.5 antisense oligonucleotide, AZD9150, decreases neuroblastoma tumorigenicity and increases chemosensitivity

2017

Abstract Purpose: Neuroblastoma is a pediatric tumor of peripheral sympathoadrenal neuroblasts. The long-term event-free survival of children with high-risk neuroblastoma is still poor despite the improvements with current multimodality treatment protocols. Activated JAK/STAT3 pathway plays an important role in many human cancers, suggesting that targeting STAT3 is a promising strategy for treating high-risk neuroblastoma. Experimental Design: To evaluate the biologic consequences of specific targeting of STAT3 in neuroblastoma, we assessed the effect of tetracycline (Tet)-inducible STAT3 shRNA and the generation 2.5 antisense oligonucleotide AZD9150 which targets STAT3 in three representat…

0301 basic medicineSTAT3 Transcription FactorCancer Researchmedicine.disease_causeSmall hairpin RNA03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineNeuroblastomaCell Line TumorOligonucleotidemedicineSTAT3CarcinogenesiCell ProliferationCisplatinAntineoplastic Combined Chemotherapy ProtocolbiologyCell growthAnimalCancerApoptosiOligonucleotides Antisensemedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation Neoplastic030104 developmental biologyOncologyCell culture030220 oncology & carcinogenesisCancer researchbiology.proteinCisplatinCarcinogenesismedicine.drugHuman
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From Genesis to Revelation: The Role of Inflammatory Mediators in Chronic Respiratory Diseases and their Control by Nucleic Acid-based Drugs.

2015

Asthma, chronic obstructive pulmonary disease, cystic fibrosis, and idiopathic pulmonary fibrosis, are among the most common chronic diseases and their prevalence is increasing. Each of these diseases is characterized by the secretion of cytokines and pro-inflammatory molecules which are thought to play a critical role in their pathogenesis. Moreover, immune cells, particularly neutrophils, macrophages and dendritic cells as well structural cells such as epithelial and airway smooth muscle cells are also involved in the pathogenic cycle of these diseases. There is a pressing need for the development of new therapies for these pulmonary diseases, particularly as no existing treatment has bee…

0301 basic medicineSmall interfering RNARespiratory diseasessiRNA deliveryHMGB1 (high-mobility group box 1)medicine.medical_treatmentGenetic enhancementOligonucleotidesPharmaceutical Science02 engineering and technologyBiologySmall InterferingPathogenesis03 medical and health sciencesIdiopathic pulmonary fibrosisImmune systemRNA interferenceNucleic AcidsmedicineAnimalsHumansAntisenseHMGB1 ProteinRNA Small InterferingCatalyticLungNABDs deliveryDNADNA CatalyticGenetic TherapyOligonucleotides Antisense021001 nanoscience & nanotechnologymedicine.diseaseRespiration Disorders030104 developmental biologyCytokinemedicine.anatomical_structureImmunologyChronic DiseaseRNAInflammation Mediators0210 nano-technologyHMGB1 (high-mobility group box 1); Inflammation mediators; NABDs delivery; Respiratory diseases; siRNA delivery; Animals; Chronic Disease; DNA Catalytic; HMGB1 Protein; Humans; Inflammation Mediators; Nucleic Acids; Oligonucleotides Antisense; RNA Small Interfering; Respiration Disorders; Genetic TherapyCurrent drug delivery
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A detailed experimental study of a DNA computer with two endonucleases

2017

Abstract Great advances in biotechnology have allowed the construction of a computer from DNA. One of the proposed solutions is a biomolecular finite automaton, a simple two-state DNA computer without memory, which was presented by Ehud Shapiro’s group at the Weizmann Institute of Science. The main problem with this computer, in which biomolecules carry out logical operations, is its complexity – increasing the number of states of biomolecular automata. In this study, we constructed (in laboratory conditions) a six-state DNA computer that uses two endonucleases (e.g. AcuI and BbvI) and a ligase. We have presented a detailed experimental verification of its feasibility. We described the effe…

0301 basic medicineTheoretical computer scienceDNA LigasesComputer scienceCarry (arithmetic)Oligonucleotides0102 computer and information sciencesBioinformatics01 natural sciencesGeneral Biochemistry Genetics and Molecular Biologylaw.inventionAutomationComputers Molecular03 medical and health sciencesDNA computinglawA-DNADeoxyribonucleases Type II Site-Specificchemistry.chemical_classificationDNA ligaseFinite-state machineBase Sequencebiomolecular computers; DNA computing; finite automataProcess (computing)DNAModels TheoreticalEndonucleasesAutomaton030104 developmental biologychemistry010201 computation theory & mathematicsWord (computer architecture)Zeitschrift für Naturforschung C
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Dom34 Links Translation to Protein O-mannosylation.

2016

In eukaryotes, Dom34 upregulates translation by securing levels of activatable ribosomal subunits. We found that in the yeast Saccharomyces cerevisiae and the human fungal pathogen Candida albicans, Dom34 interacts genetically with Pmt1, a major isoform of protein O-mannosyltransferase. In C. albicans, lack of Dom34 exacerbated defective phenotypes of pmt1 mutants, while they were ameliorated by Dom34 overproduction that enhanced Pmt1 protein but not PMT1 transcript levels. Translational effects of Dom34 required the 5′-UTR of the PMT1 transcript, which bound recombinant Dom34 directly at a CA/AC-rich sequence and regulated in vitro translation. Polysomal profiling revealed that Dom34 stimu…

0301 basic medicineUntranslated regionCancer ResearchGlycosylationMolecular biologyHydrolasesOligonucleotidesGene ExpressionRNA-binding proteinCell Cycle ProteinsYeast and Fungal ModelsPathology and Laboratory MedicineMannosyltransferasesBiochemistryTranscription (biology)Untranslated RegionsCandida albicansMedicine and Health SciencesProtein IsoformsGenetics (clinical)CandidaFungal PathogensNucleotidesMessenger RNACell biologyEnzymesNucleic acidsDenaturationPhenotypesPhenotypeMedical MicrobiologySaccharomyces CerevisiaePathogensResearch ArticleGene isoformSaccharomyces cerevisiae Proteinslcsh:QH426-470NucleasesSaccharomyces cerevisiaeMycologyBiologyResearch and Analysis MethodsMicrobiology03 medical and health sciencesSaccharomycesModel OrganismsRibonucleasesDownregulation and upregulationEndoribonucleasesDNA-binding proteinsGeneticsHumansGeneMicrobial PathogensEcology Evolution Behavior and Systematics030102 biochemistry & molecular biologyOrganismsFungiBiology and Life SciencesProteinsRibosomal RNAbiology.organism_classificationMolecular biologyYeastRNA denaturationlcsh:Genetics030104 developmental biologyMolecular biology techniquesProtein BiosynthesisEnzymologyRNAProtein TranslationRibosomesPLoS Genetics
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Selective α-synuclein knockdown in monoamine neurons by intranasal oligonucleotide delivery: potential therapy for parkinson’s disease

2018

Progressive neuronal death in brainstem nuclei and widespread accumulation of α-synuclein are neuropathological hallmarks of Parkinson’s disease (PD). Reduction of α-synuclein levels is therefore a potential therapy for PD. However, because α-synuclein is essential for neuronal development and function, α-synuclein elimination would dramatically impact brain function. We previously developed conjugated small interfering RNA (siRNA) sequences that selectively target serotonin (5-HT) or norepinephrine (NE) neurons after intranasal administration. Here, we used this strategy to conjugate inhibitory oligonucleotides, siRNA and antisense oligonucleotide (ASO), with the triple monoamine reuptake …

0301 basic medicineanimal diseasesDopamineOligonucleotidesGene ExpressionPharmacologySynaptic TransmissionPrefrontal cortexMiceDA neurotransmission0302 clinical medicineDrug DiscoveryMonoaminergicNeural PathwaysRNA Small InterferingCells Cultured5-HT neurotransmissionChemistryGene Transfer TechniquesParkinson DiseaseVentral tegmental areaSubstantia Nigramedicine.anatomical_structureCaudate putamenGene Knockdown Techniquesalpha-SynucleinMolecular MedicineRNA InterferenceOriginal ArticleMonoamine reuptake inhibitormedicine.drugSignal TransductionSerotoninSubstantia nigraASO03 medical and health sciencesProsencephalonα-synucleinDopamineIntranasal administrationGeneticsmedicineAnimalsHumansMolecular BiologyAdministration IntranasalPharmacologyPars compactaDopaminergic NeuronsGenetic TherapyCorpus Striatumnervous system diseases030104 developmental biologyMonoamine neurotransmitterGene Expression Regulationnervous systemsiRNAParkinson’s diseaseLocus coeruleus030217 neurology & neurosurgery
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Therapeutic Potential of AntagomiR-23b for Treating Myotonic Dystrophy

2020

Myotonic dystrophy type 1 (DM1) is a chronically debilitating, rare genetic disease that originates from an expansion of a noncoding CTG repeat in the dystrophia myotonica protein kinase (DMPK) gene. The expansion becomes pathogenic when DMPK transcripts contain 50 or more repetitions due to the sequestration of the muscleblind-like (MBNL) family of proteins. Depletion of MBNLs causes alterations in splicing patterns in transcripts that contribute to clinical symptoms such as myotonia and muscle weakness and wasting. We previously found that microRNA (miR)-23b directly regulates MBNL1 in DM1 myoblasts and mice and that antisense technology (“antagomiRs”) blocking this microRNA (miRNA) boost…

0301 basic medicinemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesMyotonic dystrophyArticleantagomiR03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDrug DiscoverymicroRNAMedicineMBNL1AntagomirProtein kinase AmiRNAmyotonic dystrophybusiness.industrylcsh:RM1-950Muscle weaknessmedicine.diseaseMyotoniaMbnl1030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisRNA splicingCancer researchHSALR miceMolecular Medicinemedicine.symptomDM1antisense oligonucleotidesbusinessMolecular Therapy: Nucleic Acids
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Cytochrome P450 regulation by hepatocyte nuclear factor 4 in human hepatocytes: A study using adenovirus-mediated antisense targeting

2001

Abstract Hepatocyte nuclear factor 4 (HNF4) is a member of the nuclear receptor super-family that has shown activating effects on particular cytochrome P450 (CYP) promoters from several species. However, its role in the regulation of human CYPs in the liver is still poorly understood, as no comprehensive studies in human-relevant models have been performed. In the present study, we have investigated whether HNF4 plays a general role in the expression of 7 major CYP genes in primary cultured human hepatocytes. To this end, we developed an adenoviral vector for efficient expression of HNF4 antisense RNA. Transduction of human hepatocytes with the recombinant adenovirus resulted in a time-depe…

AdultMaleGene ExpressionBiologymedicine.disease_causeAdenoviridaeCytochrome P-450 Enzyme SystemGene expressionmedicineHumansRNA MessengerTranscription factorCells CulturedAgedMessenger RNAExpression vectorHepatologyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMiddle AgedOligonucleotides AntisensePhosphoproteinsMolecular biologyAntisense RNADNA-Binding Proteinsbody regionsAdenoviridaeHepatocyte Nuclear Factor 4LiverHepatocyte nuclear factor 4Nuclear receptorGene TargetingHepatocytesRNAFemaleTranscription FactorsHepatology
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