Search results for "gene knockdown"

showing 10 items of 174 documents

Nupr1-Aurora Kinase A Pathway Provides Protection against Metabolic Stress-Mediated Autophagic-Associated Cell Death

2012

Abstract Purpose: The limited supply of oxygen and nutrients is thought to result in rigorous selection of cells that will eventually form the tumor. Experimental Design: Nupr1 expression pattern was analyzed in human tissue microarray (TMA) and correlated with survival time of the patient. Microarray analysis was conducted on MiaPaCa2 cells subjected to metabolic stress in Nupr1-silenced conditions. DNA repair and cell cycle–associated gene expression was confirmed by real-time quantitative PCR (qRT-PCR). Nupr1 and AURKA protective role were analyzed using RNA interference (RNAi) silencing or overexpression. DNA damage and autophagy were analyzed by Western blot analysis and immunofluoresc…

Cancer ResearchProgrammed cell deathCell SurvivalDNA damageDNA repairAdenocarcinomaProtein Serine-Threonine KinasesBiologyAurora KinasesStress PhysiologicalCell Line TumorAutophagyBasic Helix-Loop-Helix Transcription FactorsHumansGene silencingAurora Kinase ARegulation of gene expressionGene knockdownMicroarray analysis techniquesAURKA GeneMolecular biologyCell HypoxiaNeoplasm ProteinsCell biologyGene Expression Regulation NeoplasticGlucoseOncologyRNA InterferenceCarcinoma Pancreatic DuctalClinical Cancer Research
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HIF-1 is involved in the negative regulation of AURKA expression in breast cancer cell lines under hypoxic conditions

2013

Numerous microarray-based gene expression studies performed on several types of solid tumors revealed significant changes in key genes involved in progression and regulation of the cell cycle, including AURKA that is known to be overexpressed in many types of human malignancies. Tumor hypoxia is associated with poor prognosis in several cancer types, including breast cancer (BC). Since hypoxia is a condition that influences the expression of many genes involved in tumorigenesis, proliferation, and cell cycle regulation, we performed a microarray-based gene expression analysis in order to identify differentially expressed genes in BC cell lines exposed to hypoxia. This analysis showed that h…

Cancer ResearchSettore MED/06 - Oncologia MedicaDown-RegulationBreast NeoplasmsBiologymedicine.disease_causeAURKA Breast cancer Cell cycle HIF-1a HypoxiaCell Line TumorGene expressionTranscriptional regulationmedicineHumansPromoter Regions GeneticAurora Kinase ARegulation of gene expressionGene knockdownTumor hypoxiaCell cycleHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitMolecular biologyCell HypoxiaGene Expression Regulation NeoplasticOncologyGene Knockdown TechniquesCancer researchFemalemedicine.symptomCarcinogenesisBreast Cancer Research and Treatment
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Rad51 and BRCA2 - New Molecular Targets for Sensitizing Glioma Cells to Alkylating Anticancer Drugs

2011

First line chemotherapeutics for brain tumors (malignant gliomas) are alkylating agents such as temozolomide and nimustine. Despite growing knowledge of how these agents work, patients suffering from this malignancy still face a dismal prognosis. Alkylating agents target DNA, forming the killing lesion O(6)-alkylguanine, which is converted into DNA double-strand breaks (DSBs) that trigger apoptosis. Here we assessed whether inhibiting repair of DSBs by homologous recombination (HR) or non-homologous end joining (NHEJ) is a reasonable strategy for sensitizing glioma cells to alkylating agents. For down-regulation of HR in glioma cells, we used an interference RNA (iRNA) approach targeting Ra…

Cancer Treatmentlcsh:MedicineApoptosisToxicologyBiochemistrychemistry.chemical_compoundDrug DiscoveryRNA Small Interferinglcsh:ScienceHomologous RecombinationNeurological TumorsGene knockdownMultidisciplinaryBrain NeoplasmsGliomaFlow CytometryNon-homologous end joiningOncologyPARP inhibitorMedicinemedicine.drugResearch ArticleBiotechnologyDrugs and DevicesDrug Research and DevelopmentDNA damageMorpholinesToxic AgentsOlaparibGliomaCell Line TumormedicineHumansBiologyAntineoplastic Agents AlkylatingProtein Kinase InhibitorsBRCA2 ProteinTemozolomideBase SequenceNimustinelcsh:RCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseasechemistryMicroscopy FluorescenceChromonesCancer researchlcsh:QRad51 RecombinaseDNA DamagePLoS ONE
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Changes in carnitine octanoyltransferase activity induce alteration in fatty acid metabolism

2011

The peroxisomal beta oxidation of very long chain fatty acids (VLCFA) leads to the formation of medium chain acyl-CoAs such as octanoyl-CoA. Today, it seems clear that the exit of shortened fatty acids produced by the peroxisomal beta oxidation requires their conversion into acyl-carnitine and the presence of the carnitine octanoyltransferase (CROT). Here, we describe the consequences of an overexpression and a knock down of the CROT gene in terms of mitochondrial and peroxisomal fatty acids metabolism in a model of hepatic cells. Our experiments showed that an increase in CROT activity induced a decrease in MCFA and VLCFA levels in the cell. These changes are accompanied by an increase in …

CellBiophysicsOxidative phosphorylationBiochemistrychemistry.chemical_compoundPeroxisomesmedicineHumansCarnitineRNA Small InterferingMolecular Biologychemistry.chemical_classificationFatty acid metabolismFatty AcidsHep G2 CellsCell BiologyMetabolismPeroxisomeHEK293 Cellsmedicine.anatomical_structureEnzymeCarnitine AcyltransferaseschemistryBiochemistryGene Knockdown TechniquesHepatic stellate cellOxidation-Reductionmedicine.drugBiochemical and Biophysical Research Communications
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EphrinB2 controls vessel pruning through STAT1-JNK3 signalling

2014

Angiogenesis produces primitive vascular networks that need pruning to yield hierarchically organized and functional vessels. Despite the critical importance of vessel pruning to vessel patterning and function, the mechanisms regulating this process are not clear. Here we show that EphrinB2, a well-known player in angiogenesis, is an essential regulator of endothelial cell death and vessel pruning. This regulation depends upon phosphotyrosine-EphrinB2 signalling repressing c-jun N-terminal kinase 3 activity via STAT1. JNK3 activation causes endothelial cell death. In the absence of JNK3, hyaloid vessel physiological pruning is impaired, associated with abnormal persistence of hyaloid vessel…

Chromatin ImmunoprecipitationCell SurvivalAngiogenesisImmunoblottingRegulatorFluorescent Antibody TechniqueNeovascularization PhysiologicGeneral Physics and AstronomyEphrin-B2Persistent Hyperplastic Primary VitreousIn Vitro TechniquesBiologyBioinformaticsMicrophthalmiaArticleGeneral Biochemistry Genetics and Molecular BiologyNeovascularizationMiceMitogen-Activated Protein Kinase 10Human Umbilical Vein Endothelial CellsmedicineAnimalsHumansImmunoprecipitationInvolution (medicine)Pruning (decision trees)Cell ProliferationMice KnockoutMultidisciplinaryNeovascularization PathologicfungiEndothelial CellsRetinal VesselsGeneral ChemistryFlow Cytometrymedicine.diseaseCell biologyEndothelial stem cellSTAT1 Transcription Factornervous systemPersistent hyperplastic primary vitreousGene Knockdown Techniquescardiovascular systemmedicine.symptomSignal TransductionNature Communications
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Targeting components of the alternative NHEJ pathway sensitizes KRAS mutant leukemic cells to chemotherapy.

2014

Abstract Activating KRAS mutations are detected in a substantial number of hematologic malignancies. In a murine T-cell acute lymphoblastic leukemia (T-ALL) model, we previously showed that expression of oncogenic Kras induced a premalignant state accompanied with an arrest in T-cell differentiation and acquisition of somatic Notch1 mutations. These findings prompted us to investigate whether the expression of oncogenic KRAS directly affects DNA damage repair. Applying divergent, but complementary, genetic approaches, we demonstrate that the expression of KRAS mutants is associated with increased expression of DNA ligase 3α, poly(ADP-ribose) polymerase 1 (PARP1), and X-ray repair cross-comp…

DNA RepairImmunologyAntineoplastic AgentsApoptosisMice TransgenicBiologymedicine.disease_causePrecursor T-Cell Lymphoblastic Leukemia-LymphomaBiochemistryProto-Oncogene Proteins p21(ras)chemistry.chemical_compoundXRCC1MicePARP1Transduction GeneticmedicineAnimalsHumansDNA Breaks Double-Strandedchemistry.chemical_classificationGeneticsDNA ligaseMutationGene knockdownCell BiologyHematologyImmunohistochemistryComet assayMice Inbred C57BLDisease Models AnimalchemistryMutationCancer researchKRASComet AssayDNABlood
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Excision of Uracil from Transcribed DNA Negatively Affects Gene Expression

2014

Uracil is an unavoidable aberrant base in DNA, the repair of which takes place by a highly efficient base excision repair mechanism. The removal of uracil from the genome requires a succession of intermediate products, including an abasic site and a single strand break, before the original DNA structure can be reconstituted. These repair intermediates are harmful for DNA replication and also interfere with transcription under cell-free conditions. However, their relevance for cellular transcription has not been proved. Here we investigated the influence of uracil incorporated into a reporter vector on gene expression in human cells. The expression constructs contained a single uracil opposi…

DNA RepairTranscription GeneticGreen Fluorescent ProteinsGene ExpressionDNA and ChromosomesBiologyBiochemistryCell LineDNA Glycosylaseschemistry.chemical_compoundGenes ReporterActivation-induced (cytidine) deaminaseHumansheterocyclic compoundsProtein–DNA interactionAP siteUracilUracil-DNA GlycosidaseMolecular BiologyUracilDNACell BiologyBase excision repairMolecular biologyThymine DNA GlycosylasechemistryDNA glycosylaseGene Knockdown TechniquesUracil-DNA glycosylasebiology.proteinHeLa CellsNucleotide excision repairJournal of Biological Chemistry
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Metabolic and Functional Genomic Studies Identify Deoxythymidylate Kinase as a target in LKB1 Mutant Lung Cancer

2013

Abstract The LKB1/STK11 tumor suppressor encodes a serine/threonine kinase, which coordinates cell growth, polarity, motility, and metabolism. In non–small cell lung carcinoma, LKB1 is somatically inactivated in 25% to 30% of cases, often concurrently with activating KRAS mutations. Here, we used an integrative approach to define novel therapeutic targets in KRAS-driven LKB1-mutant lung cancers. High-throughput RNA interference screens in lung cancer cell lines from genetically engineered mouse models driven by activated KRAS with or without coincident Lkb1 deletion led to the identification of Dtymk, encoding deoxythymidylate kinase (DTYMK), which catalyzes dTTP biosynthesis, as synthetica…

DNA Replicationcongenital hereditary and neonatal diseases and abnormalitiesLung NeoplasmsMutantSTK11BiologyAMP-Activated Protein KinasesProtein Serine-Threonine Kinasesmedicine.disease_causeArticleProto-Oncogene Proteins p21(ras)MiceDeoxythymidylate kinaseAMP-Activated Protein Kinase KinasesRNA interferenceCell Line TumorCarcinoma Non-Small-Cell LungmedicineMetabolomicsThymine NucleotidesAnimalsHumansMolecular Targeted TherapyLung cancerskin and connective tissue diseasesCell DeathModels GeneticKinaseCell growthGenomicsmedicine.diseaseMolecular biologyHigh-Throughput Screening AssaysOncologyGene Knockdown TechniquesCancer researchRNA InterferenceKRASNucleoside-Phosphate KinaseDNA Damage
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Spontaneous Epileptic Manifestations in a DCX Knockdown Model of Human Double Cortex

2010

Previous reports indicate that in utero knockdown of doublecortin (DCX) results in the genesis of a subcortical heterotopia reminiscent of the doublecortex observed in female patients with DCX mutations. It has also been shown that these rats display an increased susceptibility to convulsant agents and increased cortical neurons excitability; but it is presently unknown whether they display spontaneous seizures. Furthermore, the link between the size of heterotopia and the clinical manifestation remained to be elucidated. Using video--electrocorticogram recordings, we now report that DCX knockdown induces frequent spontaneous seizures commonly associated with myoclonic jerks in adult rats. …

Doublecortin Domain ProteinsMalePathologymedicine.medical_specialtyDoublecortin ProteinCognitive NeuroscienceMyoclonic JerkClinical manifestationCellular and Molecular NeuroscienceEpilepsymedicineAnimalsHumansRats WistarHeterotopia (space)Gene knockdownEpilepsybiologyNeuropeptidesmedicine.diseaseRatsDoublecortinMalformations of Cortical DevelopmentDisease Models AnimalAnimals NewbornIn uteroGene Knockdown TechniquesConvulsantbiology.proteinFemalePsychologyMicrotubule-Associated ProteinsCerebral Cortex
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Early asymmetric cues triggering the dorsal/ventral gene regulatory network of the sea urchin embryo

2014

Dorsal/ventral (DV) patterning of the sea urchin embryo relies on a ventrally-localized organizer expressing Nodal, a pivotal regulator of the DV gene regulatory network. However, the inceptive mechanisms imposing the symmetry-breaking are incompletely understood. In Paracentrotus lividus, the Hbox12 homeodomain-containing repressor is expressed by prospective dorsal cells, spatially facing and preceding the onset of nodal transcription. We report that Hbox12 misexpression provokes DV abnormalities, attenuating nodal and nodal-dependent transcription. Reciprocally, impairing hbox12 function disrupts DV polarity by allowing ectopic expression of nodal. Clonal loss-of-function, inflicted by b…

Embryo NonmammalianTranscription GeneticEctodermp38 Mitogen-Activated Protein Kinasessymmetry breakingdorsal ventral axis sea urchin embryo nodal homeodomain repressor p38 MAPKAnimals Genetically ModifiedCell polarityMorphogenesisGene Regulatory NetworksBiology (General)ZebrafishSea urchinsea urchin embryoGeneticsbiologyGeneral NeuroscienceQRdorsal/ventral polarityCell PolarityGene Expression Regulation DevelopmentalEmbryoGeneral MedicineCell biologymedicine.anatomical_structureGene Knockdown Techniquesembryonic structuresParacentrotusMedicineCuesResearch Articleanimal structuresQH301-705.5Nodal ProteinScienceEmbryonic DevelopmentSettore BIO/11 - Biologia Molecolarep38 MAPKModels BiologicalGeneral Biochemistry Genetics and Molecular Biologybiology.animalEctodermmedicineAnimalsBody PatterningHomeodomain ProteinsGeneral Immunology and MicrobiologyotherCell Biologybiology.organism_classificationEmbryonic stem cellhomeodomain repressorRepressor ProteinsDevelopmental Biology and Stem CellsnodalNODALDevelopmental biologyeLife
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