Search results for "RNA interference"

showing 10 items of 202 documents

Murine liver organoids as a genetically flexible system to study liver cancer in vivo and in vitro.

2019

The rising incidence of cholangiocarcinoma (CCA) coupled with a low 5-year survival rate that remains below 10% delineates the urgent need for more effective treatment strategies. Although several recent studies provided detailed information on the genetic landscape of this fatal malignancy, versatile model systems to functionally dissect the immediate clinical relevance of the identified genetic alterations are still missing. To enhance our understanding of CCA pathophysiology and facilitate rapid functional annotation of putative CCA driver and tumor maintenance genes, we developed a tractable murine CCA model by combining the cyclization recombination (Cre)-lox system, RNA interference, …

TransplantationHepatologyCas9RNA interferencemedicineOrganoidCancer researchCRISPRContext (language use)BiologyLiver cancermedicine.diseasePhenotype
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Human Papilloma Virus-Dependent HMGA1 Expression Is a Relevant Step in Cervical Carcinogenesis

2008

HMGA1 is a member of a small family of architectural transcription factors involved in the coordinate assembly of multiprotein complexes referred to as enhanceosomes. In addition to their role in cell proliferation, differentiation, and development, high-mobility group proteins of the A type (HMGA) family members behave as transforming protoncogenes either in vitro or in animal models. Recent reports indicated that HMGA1 might counteract p53 pathway and provided an interesting hint on the mechanisms determining HMGA's transforming potential. HMGA1 expression is deregulated in a very large array of human tumors, including cervical cancer, but very limited information is available on the mole…

Uterine Cervical NeoplasmCancer ResearchDNA-Binding ProteinBiologyHeLa Celllcsh:RC254-282DNA-binding proteinRNA interferenceCell Line TumorHMGA1a ProteinRNA MessengerReceptor Notch1PapillomaviridaePapillomavirus InfectionPsychological repressionTranscription factorCell ProliferationReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingHMGAOncogene Proteins ViralCell Transformation Virallcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHMGA1Gene Expression Regulation NeoplasticGene expression profilingCancer cellCancer researchbiology.proteinFemaleTumor Suppressor Protein p53HumanNeoplasia
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Protein kinase C   promotes angiogenic activity of human endothelial cells via induction of vascular endothelial growth factor

2008

Aims Protein kinase C (PKC) plays an important role in the regulation of angiogenesis. However, downstream targets of PKC in endothelial cells are poorly defined. Methods and results mRNA expression of vascular endothelial growth factor (VEGF) was analysed by quantitative real-time RT-PCR in human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 cells. siRNA was used to knockdown PKC isoforms and VEGF. Matrigel tube formation assay was used to analyse the angiogenic activity of endothelial cells. Phorbol-12-myristate-13-acetate (PMA) enhanced the ability of HUVEC to organize into tubular networks when plated on Matrigel, a phenomenon that could be prevented by PKC inhibi…

Vascular Endothelial Growth Factor Amedicine.medical_specialtyProtein Kinase C-alphaTime FactorsPhysiologyAngiogenesismedicine.medical_treatmentBlotting WesternCarbazolesNeovascularization PhysiologicBiologyPolymerase Chain ReactionCell Linechemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansRNA MessengerRNA Small InterferingCell ShapeProtein Kinase InhibitorsCells CulturedProtein kinase CTube formationMatrigelStem CellsGrowth factorEndothelial CellsUp-RegulationCell biologyEnzyme ActivationEndothelial stem cellVascular endothelial growth factorAutocrine CommunicationVascular endothelial growth factor AReceptors Vascular Endothelial Growth FactorEndocrinologychemistryTetradecanoylphorbol AcetateAngiogenesis Inducing AgentsFibroblast Growth Factor 2RNA InterferenceCardiology and Cardiovascular MedicineCardiovascular Research
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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RNAi assays in the model fungus Hebeloma cylindrosporum

2007

International audience; Posttranscriptional gene silencing is a mechanism of suppressing gene expression in a sequence specific manner. This naturally occurring phenomenon of RNA interference (RNAi) has been used by researchers for gene function analysis in plants, fungi and animals. There is currently no report on RNAi establishment in mycorrhizal fungi. In order to obtain an insight into the in-vivo function of recently described genes coding for transporters and enzymes involved in N uptake and metabolism (Müller et al., 2007) from H. cylindrosporum, it is necessary to establish several methods for genetic analysis. After successfully expressing an EGFP in the mycelium of H.c. (Müller et…

[SDV] Life Sciences [q-bio][SDV]Life Sciences [q-bio]RNA INTERFERENCEfungi
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Plexin-B1 activates NF-κB and IL-8 to promote a pro-angiogenic response in endothelial cells.

2011

Background The semaphorins and their receptors, the plexins, are proteins related to c-Met and the scatter factors that have been implicated in an expanding signal transduction network involving co-receptors, RhoA and Ras activation and deactivation, and phosphorylation events. Our previous work has demonstrated that Semaphorin 4D (Sema4D) acts through its receptor, Plexin-B1, on endothelial cells to promote angiogenesis in a RhoA and Akt-dependent manner. Since NF-κB has been linked to promotion of angiogenesis and can be activated by Akt in some contexts, we wanted to examine NF-κB in Sema4D treated cells to determine if there was biological significance for the pro-angiogenic phenotype o…

animal structuresRHOAProto-Oncogene Proteins c-aktAngiogenesisSignaling in cellular processesG-protein signalingCancer TreatmentSEMA4Dlcsh:MedicineSignal transductionBiology03 medical and health sciencesMolecular cell biology0302 clinical medicineSemaphorinSettore BIO/10 - BiochimicaAkt Signaling CascadeMembrane Receptor SignalingInterleukin 8lcsh:ScienceBiologyProtein kinase BGTPase signalingRas signaling030304 developmental biology0303 health sciencesMultidisciplinaryMechanisms of Signal Transductionlcsh:RSignaling Cascades3. Good healthCell biologyPlexin B1RNA interferencepro-angiogenicendothelial cellsOncology030220 oncology & carcinogenesisembryonic structuresCancer researchbiology.proteinMedicinelcsh:QAntiangiogenesis TherapyAntiapoptotic signalingSignal transductionResearch ArticlePLoS ONE
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Overcoming of P-glycoprotein-mediated multidrug resistance of tumors in vivo by drug combinations

2014

Summary Inhibition of P-glycoprotein represents an attractive possibility to modulate resistance of cancer cells to anticancer drugs. One major strategy to overcome P-glycoprotein-mediated multidrug resistance (MDR) of tumors is to increase intracellular concentrations of anticancer drugs. This can be achieved by blocking of P-glycoprotein-mediated drug efflux using synthetic or natural small molecules or monoclonal antibodies, which bind to various parts of the efflux channel. Another possibility to increase intracellular drug concentrations can be reached by nanoparticles. A further major strategy to overcome MDR involves the downregulation of P-glycoprotein expression either by therapeut…

biologyMedicine (miscellaneous)Cell BiologyPharmacologySmall moleculeMultiple drug resistanceRNA interferenceIn vivoCancer cellbiology.proteinPharmacology (medical)EffluxMolecular BiologyPI3K/AKT/mTOR pathwayP-glycoproteinSynergy
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MiR-221 promotes stemness of breast cancer cells by targeting DNMT3b

2016

// Giuseppina Roscigno 1, 2 , Cristina Quintavalle 1, 2 , Elvira Donnarumma 3 , Ilaria Puoti 1 , Angel Diaz-Lagares 4 , Margherita Iaboni 1 , Danilo Fiore 1 , Valentina Russo 1 , Matilde Todaro 5 , Giulia Romano 6 , Renato Thomas 7 , Giuseppina Cortino 7 , Miriam Gaggianesi 5 , Manel Esteller 4 , Carlo M. Croce 6 , Gerolama Condorelli 1, 2 1 Department of Molecular Medicine and Medical Biotechnology, “Federico II” University of Naples, Naples, Italy 2 IEOS-CNR, Naples, Italy 3 IRCCS-SDN, Naples, Italy 4 Epigenetic and Cancer Biology Program (PEBC) IDIBELL, Hospital Duran I Reynals, Barcelona, Spain 5 Department of Surgical and Oncological Sciences, Cellular and Molecular Pathophysiology Lab…

cancer stem cells0301 basic medicineMicro RNAsCellular differentiationADNDNMTStem cellsStem cell markermedicine.disease_causeBioinformaticsMCF-7 Cell0302 clinical medicineBreast cancerHEK293 CellTumor Cells CulturedDNA (Cytosine-5-)-MethyltransferasesOligonucleotide Array Sequence AnalysisMicroscopy ConfocalReverse Transcriptase Polymerase Chain ReactionMicroRNAHomeodomain ProteinNanog Homeobox ProteinmicroRNAsGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisMCF-7 CellsNeoplastic Stem CellsRNA InterferenceCèl·lules mareBreast NeoplasmResearch PaperHumanHomeobox protein NANOGBlotting WesternBreast NeoplasmsBiologyCàncer de mama03 medical and health sciencesmicroRNAs breast cancer cancer stem cells DNMTBreast cancerCancer stem cellCell Line TumorSpheroids CellularmedicineHumansHomeodomain ProteinsOligonucleotide Array Sequence AnalysiCancer stem cellGene Expression ProfilingCancerDNAmedicine.diseaseMolecular medicineMicroRNAsHEK293 Cells030104 developmental biologyDNA (Cytosine-5-)-MethyltransferaseCancer researchNeoplastic Stem CellCarcinogenesisOctamer Transcription Factor-3
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Evidence of oxidative stress in very long chain fatty acid--treated oligodendrocytes and potentialization of ROS production using RNA interference-di…

2011

X-linked adrenoleukodystrophy (X-ALD) and pseudo neonatal adrenoleukodystrophy (P-NALD) are neurodegenerative demyelinating diseases resulting from the functional loss of the peroxisomal ATP-binding cassette transporter D (ABCD1) and from single peroxisomal enzyme deficiency (Acyl-CoA oxidase1: ACOX1), respectively. As these proteins are involved in the catabolism of very long chain fatty acids (VLCFA: C24:0, C26:0), X-ALD and P-NALD patients are characterized by the accumulation of VLCFA in plasma and tissues. Since peroxisomes are involved in the metabolism of reactive oxygen species (ROS) and nitrogen species (RNS), we examined the impact of VLCFA on the oxidative status of 158N murine o…

congenital hereditary and neonatal diseases and abnormalitiesendocrine systemendocrine system diseasesVery long chain fatty acidBlotting Westernmedicine.disease_causeReal-Time Polymerase Chain ReactionTransfectionATP Binding Cassette Transporter Subfamily D Member 1Gas Chromatography-Mass SpectrometrySuperoxide dismutaseLipid peroxidationchemistry.chemical_compoundMicemedicinePeroxisomesAnimalsAdrenoleukodystrophyCells Culturedchemistry.chemical_classificationReactive oxygen speciesbiologyReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceFatty Acidsnutritional and metabolic diseasesPeroxisomemedicine.diseaseFlow CytometryOligodendrogliaOxidative StressBiochemistrychemistryGene Knockdown Techniquesbiology.proteinACOX1AdrenoleukodystrophyATP-Binding Cassette TransportersRNA InterferenceAcyl-CoA OxidaseReactive Oxygen SpeciesOxidation-ReductionOxidative stressNeuroscience
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Suppression and Replacement Gene Therapy for Autosomal Dominant Disease in a Murine Model of Dominant Retinitis Pigmentosa

2011

For dominantly inherited disorders development of gene therapies, targeting the primary genetic lesion has been impeded by mutational heterogeneity. An example is rhodopsin-linked autosomal dominant retinitis pigmentosa with over 150 mutations in the rhodopsin gene. Validation of a mutation-independent suppression and replacement gene therapy for this disorder has been undertaken. The therapy provides a means of correcting the genetic defect in a mutation-independent manner thereby circumventing the mutational diversity. Separate adeno-associated virus (AAV) vectors were used to deliver an RNA interference (RNAi)-based rhodopsin suppressor and a codon-modified rhodopsin replacement gene res…

genetic structuresGenetic enhancementMice TransgenicPolymerase Chain ReactionPhotoreceptor cellMiceRNA interferenceRetinitis pigmentosaDrug DiscoverymedicineGeneticsElectroretinographyAnimalsGeneMolecular BiologyPharmacologyGene therapy of the human retinabiologyAutosomal dominant traitGenetic Therapymedicine.diseaseMolecular biologyDisease Models Animalmedicine.anatomical_structureRhodopsinbiology.proteinMolecular MedicineOriginal Articlesense organsRetinitis PigmentosaMolecular Therapy
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