Search results for "Blastoma"

showing 10 items of 603 documents

Oxidative modification impairs SERCA activity in Drosophila and human cell models of Parkinson's disease

2021

DJ-1 is a causative gene for familial Parkinson's disease (PD) with different functions, standing out its role against oxidative stress (OS). Accordingly, PD model flies harboring a mutation in the DJ-1β gene (the Drosophila ortholog of human DJ-1) show high levels of OS markers like protein carbonylation, a common post-translational modification that may alter protein function. To increase our understanding of PD pathogenesis as well as to discover potential therapeutic targets for pharmacological intervention, we performed a redox proteomic assay in DJ-1β mutant flies. Among the proteins that showed increased carbonylation levels in PD model flies, we found SERCA, an endoplasmic reticulum…

0301 basic medicineSERCAProteomeProtein CarbonylationProtein Deglycase DJ-1MutantOxidative phosphorylationmedicine.disease_causeSarcoplasmic Reticulum Calcium-Transporting ATPasesAnimals Genetically ModifiedProtein CarbonylationNeuroblastoma03 medical and health sciences0302 clinical medicinemedicineAnimalsDrosophila ProteinsHumansMolecular BiologyMutationActivator (genetics)ChemistryEndoplasmic reticulumfungiParkinson DiseaseCell biologyDisease Models AnimalOxidative StressDrosophila melanogasterPhenotype030104 developmental biologyMutationMolecular MedicineCalciumOxidation-Reduction030217 neurology & neurosurgeryOxidative stressBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Antiproliferative Effect of Elastin-Derived Peptide VGVAPG on SH-SY5Y Neuroblastoma Cells

2019

Throughout the lifetime of humans, the amount of stem cells and the rate of cell proliferation continue to decrease. Reactive oxygen species (ROS) are one among the many factors that promote stem cell aging. Both a decrease in the level of stem cells and increase in ROS production can lead to the development of different neurodegenerative diseases. This study was conducted to determine how the VGVAPG peptide, liberated from elastin during the aging process and under pathological conditions, affects ROS production and activities of antioxidant enzymes in undifferentiated, proliferating SH-SY5Y cells. SH-SY5Y cells were maintained in Dulbecco’s modified Eagle’s medium/nutrient mixture F-12 su…

0301 basic medicineSH-SY5YProliferationEnzyme-Linked Immunosorbent AssayToxicologySH-SY5YReal-Time Polymerase Chain ReactionSuperoxide dismutase03 medical and health sciencesNeuroblastoma0302 clinical medicineSuperoxide Dismutase-1Cell Line TumorHumansCell Proliferationchemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasebiologyDose-Response Relationship DrugCell growthGeneral NeuroscienceGlutathione peroxidaseROSCatalaseCell biologyElastin-derived peptidesElastinPPAR gamma030104 developmental biologyKi-67 AntigenchemistryVGVAPGbiology.proteinOriginal ArticleStem cellReactive Oxygen SpeciesElastinOligopeptides030217 neurology & neurosurgeryFetal bovine serumNeurotoxicity Research
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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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A Shotgun Proteomics Approach Reveals a New Toxic Role for Alzheimer's Disease Aβ Peptide: Spliceosome Impairment.

2017

Proteomic changes have been described in many neurodegenerative diseases, including Alzheimer's disease (AD). However, the early events in the onset of the pathology are yet to be fully elucidated. A cell model system in which LAN5 neuroblastoma cells were incubated for a short time with a recombinant form of Aβ42 was utilized. Proteins extracted from these cells were subjected to shotgun proteomics analysis by LTQ-Orbitrap-MS followed by label-free quantitation. By bioinformatics tools we found that the most significant of those found to be up-regulated were related to cytoskeletal dynamics (Rho related) and membrane-related processes. The most significant of the down-regulated proteins we…

0301 basic medicineSpliceosomeAmyloid beta-PeptideProteomeComputational biologyDiseaseBiologyBiochemistrylaw.inventionearly events in AD03 medical and health sciencesNeuroblastoma0302 clinical medicinelawAlzheimer DiseaseCell Line TumorHumansShotgun proteomicsCytoskeletonCytoskeletonGeneticsAmyloid beta-PeptidesChemistry (all)Cell MembraneGeneral ChemistryRibosomal RNAAlzheimer's diseaseRecombinant Proteinshotgun proteomicRecombinant Proteins030104 developmental biologySpliceosomeGene Expression RegulationRNA splicingRecombinant DNASpliceosomes030217 neurology & neurosurgeryBiogenesisHumanJournal of proteome research
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Imbalance of immunological synapse-kinapse states reflects tumor escape to immunity in glioblastoma

2018

Since the proper activation of T cells requires the physical interaction with target cells through the formation of immunological synapses (IS), an alteration at this level could be a reason why tumors escape the immune response. As part of their life cycle, it is thought that T cells alternate between a static phase, the IS, and a dynamic phase, the immunological kinapse (IK), depending on high or low antigen sensing. Our investigation performed in tissue samples of human glioma shows that T cells are able to establish synapsing interactions not only with glioma tumorigenic cells, but also with stromal myeloid cells. Particularly, the IS displaying a T cell receptor-rich (TCR-rich) central…

0301 basic medicineStromal cellCD3 ComplexImmunological SynapsesT-LymphocytesT cellAntigen-Presenting CellsImmunological synapse03 medical and health sciencesImaging Three-DimensionalImmune systemAntigenGliomaTumor MicroenvironmentmedicineHumansMyeloid CellsBrain NeoplasmsChemistryGliomaGeneral Medicinemedicine.diseaseImmunological SynapsesCell biology030104 developmental biologymedicine.anatomical_structureTechnical AdvanceTumor EscapeTumor EscapeGlioblastomaJCI Insight
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Telomeres and Telomerase During Human Papillomavirus-Induced Carcinogenesis

2018

Human papillomaviruses (HPVs) belong to a small spherical virus family and are transmitted through direct contact, most often through sexual behavior. More than 200 types of HPV are known, a dozen or so of which are classified as high-risk viruses (HR HPV) and may contribute to the development of cervical cancer. HPV is a small virus with a capsid composed of L1 and L2 proteins, which are crucial for entry to the cell. The infection begins at the basal cell layer and progresses to involve cells from higher layers of the cervical epithelium. E6 and E7 viral proteins are involved in the process of carcinogenesis. They interact with suppressors of oncogenesis, including p53 and Rb proteins. Th…

0301 basic medicineTelomeraseOncogene ProteinsCarcinogenesisCellReview ArticleBiologymedicine.disease_causeRetinoblastoma ProteinVirus03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansTelomerase reverse transcriptasePapillomaviridaeTelomeraseTelomere ShorteningPharmacologyPapillomavirus InfectionsDNA replicationGeneral MedicineOncogene Proteins ViralVirus InternalizationCell Transformation ViralTelomere030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchDisease ProgressionMolecular MedicineRNAFemaleTumor Suppressor Protein p53CarcinogenesisMolecular Diagnosis & Therapy
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Rett Syndrome Mutant Neural Cells Lacks MeCP2 Immunoreactive Bands.

2016

Dysfunctions of MeCP2 protein lead to various neurological disorders such as Rett syndrome and Autism. The exact functions of MeCP2 protein is still far from clear. At a molecular level, there exist contradictory data. MeCP2 protein is considered a single immunoreactive band around 75 kDa by western-blot analysis but several reports have revealed the existence of multiple MeCP2 immunoreactive bands above and below the level where MeCP2 is expected. MeCP2 immunoreactive bands have been interpreted in different ways. Some researchers suggest that multiple MeCP2 immunoreactive bands are unidentified proteins that cross-react with the MeCP2 antibody or degradation product of MeCP2, while others…

0301 basic medicineThreonineHeredityMethyl-CpG-Binding Protein 2Genetic LinkageMutantFluorescent Antibody TechniqueSocial Scienceslcsh:MedicinePC12 CellsBiochemistryEpitopeImmunoenzyme TechniquesCell FusionNeuroblastomaFluorescence MicroscopyAnimal CellsMedicine and Health SciencesPsychologyPost-Translational ModificationPhosphorylationAmino Acidslcsh:ScienceCells CulturedCross ReactivityNeuronsStainingMicroscopyMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionOrganic CompoundsCell StainingLight MicroscopyTransfectionChemistryX-Linked TraitsSex LinkagePhysical SciencesCellular TypesResearch ArticleCell signalingCell Physiologycongenital hereditary and neonatal diseases and abnormalitiesBlotting WesternImmunologyRett syndromeBiologyReal-Time Polymerase Chain ReactionResearch and Analysis MethodsMECP203 medical and health sciencesNeurologiaAntigenHydroxyl Amino Acidsmental disordersmedicineRett SyndromeGeneticsAnimalsHumansRNA MessengerClinical GeneticsHEK 293 cellsOrganic Chemistrylcsh:RChemical CompoundsBiology and Life SciencesProteinsCell Biologymedicine.diseaseMolecular biologyRatsnervous system diseases030104 developmental biologyHEK293 CellsSpecimen Preparation and TreatmentCellular NeuroscienceMutationDevelopmental PsychologyMalaltieslcsh:QNeuroscience
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11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma

2020

High-risk 11q deleted neuroblastomas typically display undifferentiated/poorly differentiated morphology. Neuroblastoma is thought to develop from Schwann cell precursors and undifferentiated neural crest (NC) derived cells. It is therefore vital to understand mechanisms involved in the block of differentiation. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in maintenance of undifferentiated NC-derived progenitors via repression of DLG2, a tumor suppressor in neuroblastoma. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors become chromaffin cells of the adrenal gland. We …

0301 basic medicineTranscription GeneticCarcinogenesisChromaffin CellsRetinoic acidlaw.inventionNeuroblastomachemistry.chemical_compound0302 clinical medicinelawNerve Growth FactorMedicine and Health Sciencesretinoic acidAnaplastic Lymphoma Kinaselcsh:QH301-705.5NeuronsMice Inbred BALB CNeural crestCell DifferentiationPrognosisCandidate Tumor Suppressor GeneDLG2Up-RegulationCell biologyGene Expression Regulation NeoplasticERKPhenotypeTreatment Outcomemedicine.anatomical_structureFemaleChromosome Deletiontumor suppressorMAP Kinase Signaling SystemSp1 Transcription FactorSchwann cellGenetics and Molecular BiologyTretinoinBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAdrenergic AgentsCell Line TumorNeuroblastomamedicineAnimalsHumansProgenitor cellGenePsychological repressionCell ProliferationChromosomes Human Pair 11Tumor Suppressor Proteinsmedicine.disease030104 developmental biologyALKlcsh:Biology (General)chemistryTrk receptorGeneral BiochemistrySuppressorSchwann CellsGuanylate Kinases030217 neurology & neurosurgerySSRN Electronic Journal
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Rescue of Hypovitaminosis A Induces Non-Amyloidogenic Amyloid Precursor Protein (APP) Processing.

2015

Retinoic acid, the bioactive metabolite of beta-carotene or vitamin A, plays a pleiotropic, multifunctional role in vertebrate development. Studies in rodents revealed that a diet deficient in vitamin A results in a complex neonatal syndrome (the VAD syndrome), manifested in many organs. In humans, the function of retinoic acid (RA) extends into adulthood, where it has important roles in fertility, vision, and suppression of neoplastic growth. In recent years, it has also been suggested that retinoic acid might potentially act as a therapeutically relevant drug in attenuating or even preventing neurodegenerative diseases such as Alzheimer's disease (AD). Here, we report that VAD leads to an…

0301 basic medicineVitaminmedicine.medical_specialtyADAM10Retinoic acidTretinoin03 medical and health scienceschemistry.chemical_compoundADAM10 ProteinAmyloid beta-Protein PrecursorMiceNeuroblastoma0302 clinical medicineKeratolytic AgentsTretinoinInternal medicineNeuroblastomaGene expressionPresenilin-2medicineAmyloid precursor proteinAnimalsHumansGene Regulatory NetworksRats WistarCells CulturedCerebral CortexNeuronsAmyloid beta-PeptidesbiologyVitamin A Deficiencymedicine.diseaseAcitretinPeptide FragmentsVitamin A deficiencyDisease Models Animal030104 developmental biologyEndocrinologyNeurologychemistryAnimals Newbornbiology.proteinFemaleNeurology (clinical)030217 neurology & neurosurgerymedicine.drugCurrent Alzheimer research
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The soluble form of pan-RTK inhibitor and tumor suppressor LRIG1 mediates downregulation of AXL through direct protein–protein interaction in gliobla…

2019

Abstract Background Targeted approaches for inhibiting epidermal growth factor receptor (EGFR) and other receptor tyrosine kinases (RTKs) in glioblastoma (GBM) have led to therapeutic resistance and little clinical benefit, raising the need for the development of alternative strategies. Endogenous LRIG1 (Leucine-rich Repeats and ImmunoGlobulin-like domains protein 1) is an RTK inhibitory protein required for stem cell maintenance, and we previously demonstrated the soluble ectodomain of LRIG1 (sLRIG1) to potently inhibit GBM growth in vitro and in vivo. Methods Here, we generated a recombinant protein of the ectodomain of LRIG1 (sLRIG1) and determined its activity in various cellular GBM mo…

0301 basic medicinebiologyChemistryEGFRReceptor Protein-Tyrosine KinasesglioblastomaLRIG1AXLProximity ligation assayReceptor tyrosine kinase03 medical and health sciences030104 developmental biology0302 clinical medicineEctodomainDownregulation and upregulation030220 oncology & carcinogenesisBasic and Translational Investigationsbiology.proteinCancer researchreceptor tyrosine kinaseEpidermal growth factor receptorStem cellCell adhesionNeuro-oncology Advances
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