ArticleInternational journal of molecular medicine2018
Effects of ERK1/2 S-nitrosylation on ERK1/2 phosphorylation and cell survival in glioma cells.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 32 citations in OpenAlex.
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- Investigation of the impact of resveratrol on sublethal-dose ALA-PDT in glioblastoma cells.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- Nitric oxide‑mediated S‑Nitrosylation contributes to signaling transduction in human physiological and pathological status (Review).International journal of molecular medicine · 2025Review
- The effects of cannabidiol on nitric oxide synthases: a narrative review on therapeutic implications for inflammation and oxidative stress in health and disease.Journal of cannabis research · 2025Review
- Article
- Redox regulation: mechanisms, biology and therapeutic targets in diseases.Signal transduction and targeted therapy · 2025Review
- Unveiling the Role of Protein Posttranslational Modifications in Glioma Prognosis.CNS neuroscience & therapeutics · 2025Article
- The evolution of S-nitrosylation detection methodology and the role of protein S-nitrosylation in various cancers.Cancer cell international · 2024Review
- Sulfenylation of ERK1/2: A novel mechanism for SOHeliyon · 2024Article
- Redox signaling-mediated tumor extracellular matrix remodeling: pleiotropic regulatory mechanisms.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Modulation of redox homeostasis: A strategy to overcome cancer drug resistance.Frontiers in pharmacology · 2023Review
- Expression and potential role of FOSB in glioma.Frontiers in molecular neuroscience · 2022Article
- Artemisinin attenuated ischemic stroke induced cell apoptosis through activation of ERK1/2/CREB/BCL-2 signaling pathwayInternational journal of biological sciences · 2022Article
- The versatile utility of cysteine as a target for cancer treatment.Frontiers in oncology · 2022Review
- Melatonin, Its Metabolites and Their Interference with Reactive Nitrogen Compounds.Molecules (Basel, Switzerland) · 2021Review
- S-Nitrosylation in Tumor Microenvironment.International journal of molecular sciences · 2021Review
- Chronically altered NMDAR signaling in epilepsy mediates comorbid depression.Acta neuropathologica communications · 2021Article
- S-Nitroso-L-Cysteine Ameliorated Pulmonary Hypertension in the MCT-Induced Rats through Anti-ROS and Anti-Inflammatory Pathways.Oxidative medicine and cellular longevity · 2021Article
- Adsorption of miR-218 by lncRNA HOTAIR regulates PDE7A and affects glioma cell proliferation, invasion, and apoptosis.International journal of clinical and experimental pathology · 2020Article
- Potential targets of TMEM176A in the growth of glioblastoma cells.OncoTargets and therapy · 2018Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of extracellular signal‑regulated kinase 1/2 (ERK1/2) by phosphorylation modification can trigger tumor cell development in glioma. S‑nitrosylation, which refers to the covalent addition of a nitric oxide (NO) group to a cysteine (Cys) thiol, is an important post‑translational modification that occurs on numerous cancer‑associated proteins. Protein S‑nitrosylation can increase or decrease protein activity and stability, and subsequent signal transduction and cellular processes. However, the association between ERK1/2 S‑nitrosylation and ERK1/2 phosphorylation, and the effects of ERK1 S‑nitrosylation on glioma cell survival are currently unknown. U251 glioma cells were treated with NO donors sodium nitroprusside (SNP) or S‑nitrosoglutathione (GSNO). CCK8 assay was used to assess the cell viability. NO levels in the medium were detected by Griess assay. Western blot analysis and biotin switch assay were employed to detect the ERK1/2 phosphorylation and S-nitrosylation. ERK1 wild-type and mutant plasmids were constructed, and used to transfect the U251 cells. Caspase-3 western blot analysis and flow cytometry were employed to assess cell apoptosis. The present study demonstrated that treatment with the NO donors SNP or GSNO led to an increase in ERK1/2 S‑nitrosylation, and a reduction in ERK1/2 phosphorylation, which was accompanied by growth inhibition of U251 glioma cells. Mutational analysis demonstrated that Cys183 was vital for S‑nitrosylation of ERK1, and that preventing ERK1 S‑nitrosylation by replacing Cys183 with alanine partially reversed GSNO‑induced cell apoptosis, and reductions in cell viability and ERK1/2 phosphorylation. In addition, increased ERK1/2 phosphorylation was associated with decreased ERK1/2 S‑nitrosylation in human glioma tissues. These findings identified the relationship between ERK1/2 S‑nitrosylation and phosphorylation in vitro and in vivo, and revealed a novel mechanism of ERK1/2 underlying tumor cell development and apoptotic resistance of glioma.
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