0000000000303610

AUTHOR

Michal A. Zmijewski

0000-0003-2206-3531

showing 3 related works from this author

DNA strand breaks induced by nuclear hijacking of neuronal NOS as an anti-cancer effect of 2-methoxyestradiol

2015

2-Methoxyestradiol (2-ME) is a physiological metabolite of 17β-estradiol. At pharmacological concentrations, 2-ME inhibits colon, breast and lung cancer in tumor models. Here we investigated the effect of physiologically relevant concentrations of 2-ME in osteosarcoma cell model. We demonstrated that 2-ME increased nuclear localization of neuronal nitric oxide synthase, resulting in nitro-oxidative DNA damage. This in turn caused cell cycle arrest and apoptosis in osteosarcoma cells. We suggest that 2-ME is a naturally occurring hormone with potential anti-cancer properties.

Pathologymedicine.medical_specialtyneuronal nitric oxide synthaseCell cycle checkpoint2-methoxyestradiolDNA damageAntineoplastic AgentsApoptosisBone NeoplasmsNitric Oxide Synthase Type Imedicine.disease_causeNitric OxideNitric oxidechemistry.chemical_compoundReactive nitrogen specieCell Line TumormedicineHumans2-MethoxyestradiolReactive nitrogen speciesCytokinesisOsteosarcomaEstradiolbusiness.industryDNA BreaksIntracellular Signaling Peptides and ProteinsCancermedicine.diseaseReactive Nitrogen SpeciesG2 Phase Cell Cycle CheckpointsOxidative StressOncologychemistryApoptosis2-methoxyestradiol; Neuronal nitric oxide synthase; Nitric oxide; Osteosarcoma; Reactive nitrogen species; OncologyCancer researchM Phase Cell Cycle CheckpointsbusinessTumor Suppressor p53-Binding Protein 1Oxidative stressmedicine.drugResearch Paper
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The Major Heat Shock Proteins, Hsp70 and Hsp90, in 2-Methoxyestradiol-Mediated Osteosarcoma Cell Death Model

2020

2-Methoxyestradiol is one of the natural 17&beta

neuronal nitric oxide synthaseProgrammed cell death2-methoxyestradiolLactams MacrocyclicAntineoplastic AgentsBone NeoplasmsModels BiologicalArticleCatalysisHsp90 inhibitorNitric oxidelcsh:ChemistryInorganic Chemistrychemistry.chemical_compoundDownregulation and upregulationosteosarcomaHeat shock proteinBenzoquinonesAnimalsHumansDrug InteractionsHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsPhysical and Theoretical Chemistrygeldanamycinlcsh:QH301-705.5Molecular BiologySpectroscopyAntibiotics AntineoplasticbiologyOrganic ChemistryGeneral MedicineGeldanamycinHsp90Computer Science ApplicationsHsp70lcsh:Biology (General)lcsh:QD1-999chemistryCancer researchbiology.proteinInternational Journal of Molecular Sciences
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Geldanamycin-induced osteosarcoma cell death is associated with hyperacetylation and loss of mitochondrial pool of heat shock protein 60 (hsp60)

2013

Osteosarcoma is one of the most malignant tumors of childhood and adolescence that is often resistant to standard chemo- and radio-therapy. Geldanamycin and geldanamycin analogs have been recently studied as potential anticancer agents for osteosarcoma treatment. Here, for the first time, we have presented novel anticancer mechanisms of geldanamycin biological activity. Moreover, we demonstrated an association between the effects of geldanamycin on the major heat shock proteins (HSPs) and the overall survival of highly metastatic human osteosarcoma 143B cells. We demonstrated that the treatment of 143B cells with geldanamycin caused a subsequent upregulation of cytoplasmic Hsp90 and Hsp70 w…

Cell SurvivalLactams Macrocycliclcsh:MedicineApoptosisBone NeoplasmsBiologyMitochondrionMitochondrial Proteinschemistry.chemical_compoundGeldanamycin Hsp60 Osteosarcoma cellHeat shock proteinCell Line Tumorpolycyclic compoundsBenzoquinonesHumansHeat shocklcsh:ScienceCell ProliferationOsteosarcomaMultidisciplinaryAntibiotics Antineoplasticlcsh:RAcetylationChaperonin 60GeldanamycinHsp90Molecular biologyMitochondriaProtein TransportchemistryCancer cellCancer researchbiology.proteinApoptotic signaling pathwayHSP60lcsh:QDrug Screening Assays AntitumorProtein Processing Post-TranslationalResearch ArticleSignal Transduction
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