Search results for "Gene Knockdown Techniques"

showing 10 items of 83 documents

Prox1 Is Required for Oligodendrocyte Cell Identity in Adult Neural Stem Cells of the Subventricular Zone

2016

Abstract Adult neural stem cells with the ability to generate neurons and glia cells are active throughout life in both the dentate gyrus (DG) and the subventricular zone (SVZ). Differentiation of adult neural stem cells is induced by cell fate determinants like the transcription factor Prox1. Evidence has been provided for a function of Prox1 as an inducer of neuronal differentiation within the DG. We now show that within the SVZ Prox1 induces differentiation into oligodendrocytes. Moreover, we find that loss of Prox1 expression in vivo reduces cell migration into the corpus callosum, where the few Prox1 deficient SVZ-derived remaining cells fail to differentiate into oligodendrocytes. Thu…

0301 basic medicineAdult neurogenesisMice0302 clinical medicineNeural Stem CellsCell MovementLateral VentriclesPromoter Regions GeneticCells CulturedMOUSE-BRAINReceptors NotchOligodendrocytesNeurogenesisCell DifferentiationLINEAGEAnatomyOlfactory BulbNeural stem cellCell biologyNeuroepithelial cellAdult Stem CellsOligodendrogliaDIFFERENTIATIONEnhancer Elements Geneticmedicine.anatomical_structureGene Knockdown TechniquesMolecular MedicineSPINAL-CORDStem cellSUBCELLULAR-LOCALIZATIONProtein BindingAdult stem cellOLIG2NeurogenesisSubventricular zoneBiology03 medical and health sciencesNeurosphereProx1medicineAnimalsCell LineageOLFACTORY-BULBBody PatterningHomeodomain ProteinsTumor Suppressor ProteinsCell BiologyMAMMALIAN BRAINOligodendrocyte Transcription Factor 2030104 developmental biologyNeuropoiesisPROGENITOR CELLSGene Expression Regulationnervous system030217 neurology & neurosurgeryDevelopmental BiologyStem Cells
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The NSL Chromatin-Modifying Complex Subunit KANSL2 Regulates Cancer Stem-like Properties in Glioblastoma That Contribute to Tumorigenesis.

2016

KANSL2 is an integral subunit of the nonspecific lethal (NSL) chromatin-modifying complex that contributes to epigenetic programs in embryonic stem cells. In this study, we report a role for KANSL2 in regulation of stemness in glioblastoma (GBM), which is characterized by heterogeneous tumor stem-like cells associated with therapy resistance and disease relapse. KANSL2 expression is upregulated in cancer cells, mainly at perivascular regions of tumors. RNAi-mediated silencing of KANSL2 in GBM cells impairs their tumorigenic capacity in mouse xenograft models. In clinical specimens, we found that expression levels of KANSL2 correlate with stemness markers in GBM stem-like cell populations. M…

0301 basic medicineCHROMATINMaleCancer ResearchCarcinogenesisCellCell SeparationMice SCIDmedicine.disease_causeMiceCANCER STEM CELLMice Inbred NODHistone AcetyltransferasesOligonucleotide Array Sequence AnalysisBrain NeoplasmsNuclear ProteinsMiddle AgedFlow CytometryImmunohistochemistryChromatinUp-Regulationmedicine.anatomical_structureOncologyGene Knockdown TechniquesNeoplastic Stem CellsHeterograftsFemaleCIENCIAS NATURALES Y EXACTASAdultKANSLOtras Ciencias BiológicasBlotting WesternGLIOBLASTOMABiologyReal-Time Polymerase Chain ReactionArticleCiencias Biológicas03 medical and health sciencesCancer stem cellmedicineBiomarkers TumorGene silencingAnimalsHumansEpigeneticsAgedEmbryonic stem cell030104 developmental biologyCancer cellImmunologyCancer researchCarcinogenesisGlioblastomaCancer research
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Knockdown of hnRNPK leads to increased DNA damage after irradiation and reduces survival of tumor cells.

2017

Radiotherapy is an important treatment option in the therapy of multiple tumor entities among them head and neck squamous cell carcinoma (HNSCC). However, the success of radiotherapy is limited by the development of radiation resistances. Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a cofactor of p53 and represents a potential target for radio sensitization of tumor cells. In this study, we analyzed the impact of hnRNPK on the DNA damage response after gamma irradiation. By yH2AX foci analysis, we found that hnRNPK knockdown increases DNA damage levels in irradiated cells. Tumor cells bearing a p53 mutation showed increased damage levels and delayed repair. Knockdown of hnRNPK appl…

0301 basic medicineCancer ResearchDNA damageCell Survivalmedicine.medical_treatmentmedicine.disease_causeRadiation ToleranceHeterogeneous-Nuclear Ribonucleoprotein KHistones03 medical and health sciences0302 clinical medicineCell Line TumormedicineCarcinomaGene Knockdown TechniquesHumansMutationGene knockdownChemistrySquamous Cell Carcinoma of Head and NeckStem CellsGeneral Medicinemedicine.diseaseHead and neck squamous-cell carcinomaRadiation therapy030104 developmental biologyCell cultureHead and Neck Neoplasms030220 oncology & carcinogenesisGene Knockdown TechniquesCancer researchCarcinoma Squamous CellTumor Suppressor Protein p53DNA DamageCarcinogenesis
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Growth differentiation factor 15 as a radiation-induced marker in oral carcinoma increasing radiation resistance.

2015

Background Growth differentiation factor 15 (GDF15) is involved in tumor pathogenesis of oral squamous cell carcinoma (OSCC). The aim of this study was an investigation of the potential influence of GDF15 on radioresistance of OSCC cells in vitro. Methods Oral squamous cell carcinoma cell lines were irradiated with 0, 2, or 6 Gy, and GDF15 expression in the supernatant per survived cell colony was examined with ELISA. Non-irradiated and OSCC cell lines irradiated with 6 Gy were evaluated for GDF15 expression using immunofluorescent staining. For further investigation of GDF15 effects on radioresistance, a GDF15 knockdown model in a human OSCC cell line was established, and apoptotic activit…

0301 basic medicineCancer ResearchGrowth Differentiation Factor 15CellApoptosisEnzyme-Linked Immunosorbent AssayBiologymedicine.disease_causeReal-Time Polymerase Chain ReactionTransfectionPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineRadioresistanceCell Line TumormedicineCarcinomaBiomarkers TumorHumansRNA Small InterferingMouth neoplasmSquamous Cell Carcinoma of Head and Neckmedicine.diseaseMolecular biologyNeoplasm Proteinsstomatognathic diseases030104 developmental biologymedicine.anatomical_structureOtorhinolaryngologyApoptosisCell cultureTumor progressionHead and Neck Neoplasms030220 oncology & carcinogenesisCaspasesGene Knockdown TechniquesCarcinoma Squamous CellPeriodonticsMouth NeoplasmsOral SurgeryCarcinogenesisJournal of oral pathologymedicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
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The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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Visualising G-quadruplex DNA dynamics in live cells by fluorescence lifetime imaging microscopy

2020

Guanine rich regions of oligonucleotides fold into quadruple-stranded structures called G-quadruplexes (G4s). Increasing evidence suggests that these G4 structures form in vivo and play a crucial role in cellular processes. However, their direct observation in live cells remains a challenge. Here we demonstrate that a fluorescent probe (DAOTA-M2) in conjunction with fluorescence lifetime imaging microscopy (FLIM) can identify G4s within nuclei of live and fixed cells. We present a FLIM-based cellular assay to study the interaction of non-fluorescent small molecules with G4s and apply it to a wide range of drug candidates. We also demonstrate that DAOTA-M2 can be used to study G4 stability i…

0301 basic medicineFluorescence-lifetime imaging microscopyIndolesIntravital MicroscopyGuanineScienceGeneral Physics and Astronomy010402 general chemistryG-quadruplex01 natural sciencesGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health scienceschemistry.chemical_compoundMiceCell Line TumorAnimalsHumans030304 developmental biologyFluorescent Dyes0303 health sciencesMultidisciplinaryChemistryOligonucleotideCellular AssayQDNA HelicasesGeneral ChemistryDNAFibroblastsFluorescenceSmall moleculeChemical biologyFanconi Anemia Complementation Group Proteins0104 chemical sciencesMolecular ImagingG-QuadruplexesDNA helicase activity030104 developmental biologyMicroscopy FluorescenceGene Knockdown TechniquesBiophysicsFluorescent probesMolecular imagingRNA HelicasesNature Communications
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ZNF518B gene up-regulation promotes dissemination of tumour cells and is governed by epigenetic mechanisms in colorectal cancer

2019

AbstractMost of colorectal cancer CRC-related death is due to metastasis and the finding of markers for prognosis of invasiveness, constitutes an appealing challenge. Here, after analysing cDNA array containing 43 tumour and 5 normal mucosa samples, we report that the expression of the ZNF518B gene as a whole and that of its two major splicing isoforms are significantly increased in tumours. The canonical isoform was also up-regulated in a patients’ cohort containing 70 tumour and 69 adjacent tissue samples. The effects of silencing ZNF518B on the phenotype of CRC cell lines were then studied. The gene does not affect cell proliferation, but plays a significant role in cell migration and in…

0301 basic medicineGene isoformEpithelial-Mesenchymal TransitionCelllcsh:MedicineBiologyArticleHistone DeacetylasesEpigenesis GeneticHistones03 medical and health sciences0302 clinical medicineCell MovementCell Line TumorGene expressionmedicineGene silencingHumansProtein IsoformsEpigeneticsNeoplasm Metastasislcsh:ScienceGeneCell ProliferationNeoplasm StagingMultidisciplinaryGene Expression Profilinglcsh:RPrognosisColorectal cancer3. Good healthDNA-Binding ProteinsGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structureHistoneGene Knockdown TechniquesCancer researchbiology.proteinH3K4me3lcsh:QEpigeneticsColorectal Neoplasms030217 neurology & neurosurgeryScientific Reports
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Inducible knockdown of procollagen I protects mice from liver fibrosis and leads to dysregulated matrix genes and attenuated inflammation.

2017

Organ fibrosis is characterized by a chronic wound-healing response, with excess deposition of extracellular matrix components. Here, collagen type I represents the most abundant scar component and a primary target for antifibrotic therapies. Liver fibrosis can progress to cirrhosis and primary liver cancer, which are the major causes of liver related morbidity and mortality. However, a (pro-)collagen type I specific therapy remains difficult and its therapeutic abrogation may incur unwanted side effects. We therefore designed tetracycline-regulated procollagen alpha1(I) short hairpin (sh)RNA expressing mice that permit a highly efficient inducible knockdown of the procollagen alpha1(I) gen…

0301 basic medicineGenetically modified mouseLiver CirrhosisPathologymedicine.medical_specialtyCirrhosisInflammationMice TransgenicCollagen Type ISmall hairpin RNAExtracellular matrix03 medical and health sciencesMiceFibrosismedicineAnimalsRNA Small InterferingMolecular BiologyCells CulturedGene knockdownExtracellular Matrix ProteinsChemistryMouse Embryonic Stem CellsFibroblastsmedicine.diseaseProcollagen peptidaseDisease Models Animal030104 developmental biologyGene Expression RegulationGene Knockdown TechniquesCancer researchmedicine.symptomProcollagenMatrix biology : journal of the International Society for Matrix Biology
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Hepatitis B Virus Subverts the Autophagy Elongation Complex Atg5-12/16L1 and Does Not Require Atg8/LC3 Lipidation for Viral Maturation

2018

ABSTRACT Previous studies indicated that hepatitis B virus (HBV) stimulates autophagy to favor its production. To understand how HBV co-opts autophagy as a proviral machinery, we studied the roles of key autophagy proteins in HBV-replicating liver cell cultures. RNA interference-mediated silencing of Atg5, Atg12, and Atg16L1, which promote autophagophore expansion and LC3 membrane conjugation, interfered with viral core/nucleocapsid (NC) formation/stability and strongly diminished virus yields. Concomitantly, the core/NC membrane association and their sorting to envelope-positive compartments were perturbed. A close inspection of the HBV/autophagy cross talk revealed that the virus depended…

0301 basic medicineHepatitis B virusATG8Autophagosome maturationImmunologyATG5Autophagy-Related ProteinsBiologymedicine.disease_causeVirus ReplicationMicrobiologyVirusAutophagy-Related Protein 5ATG1203 medical and health sciencesVirologyCell Line TumormedicineAutophagyHumansHepatitis B virusAutophagyAutophagy-Related Protein 8 FamilyHepatitis BCell biologyVirus-Cell Interactions030104 developmental biologyViral replicationInsect ScienceGene Knockdown TechniquesMultiprotein ComplexesMicrotubule-Associated ProteinsAutophagy-Related Protein 12
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The Cytoskeletal Adaptor Obscurin-Like 1 Interacts with the Human Papillomavirus 16 (HPV16) Capsid Protein L2 and Is Required for HPV16 Endocytosis.

2016

ABSTRACT The human papillomavirus (HPV) capsid protein L2 is essential for viral entry. To gain a deeper understanding of the role of L2, we searched for novel cellular L2-interacting proteins. A yeast two-hybrid analysis uncovered the actin-depolymerizing factor gelsolin, the membrane glycoprotein dysadherin, the centrosomal protein 68 (Cep68), and the cytoskeletal adaptor protein obscurin-like 1 protein (OBSL1) as putative L2 binding molecules. Pseudovirus (PsV) infection assays identified OBSL1 as a host factor required for gene transduction by three oncogenic human papillomavirus types, HPV16, HPV18, and HPV31. In addition, we detected OBSL1 expression in cervical tissue sections and no…

0301 basic medicineKeratinocytesvirusesImmunologyEndocytic cycleEndocytosisMicrobiologyClathrinCell Line03 medical and health sciencesTransduction (genetics)TetraspaninViral entryVirologyTwo-Hybrid System TechniquesCaveolinHumansHuman papillomavirus 16biologyPapillomavirus InfectionsSignal transducing adaptor proteinOncogene Proteins ViralVirus InternalizationEndocytosisCell biologyVirus-Cell InteractionsCytoskeletal Proteins030104 developmental biologyInsect ScienceGene Knockdown TechniquesHost-Pathogen Interactionsbiology.proteinCapsid ProteinsHeLa CellsJournal of virology
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