ArticleCancers2022
Targeting Glioblastoma via Selective Alteration of Mitochondrial Redox State.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- p53-Dependent ENOX2 Downregulation Mediates the Apoptotic Responses to Heteroarene-Fused Anthraquinones in Colon Cancer Cells.Biomolecules · 2026Article
- Phenazine Methosulfate Rewires Mitochondrial Redox Circuits to Restore Membrane Potential and ATP Synthesis Under ETC Blockade in Glioblastoma Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Why is the tumor microenvironment disordered by NADH/NADRedox biology · 2026Review
- In vivo characterization of the redox balance in IDH-wildtype glioblastomas: a J-difference edited MEGA-sLASER MRS study at 3T.Cancer & metabolism · 2026Article
- The Anti-proliferative Effects of Anandamide and Oleamide in Glioblastoma Cell Lines Recruit Mitochondrial and PPAR-γ Receptor Modulation.Neurochemical research · 2026Article
- Epigenetic and mitoepigenetic regulation in cancer and therapeutic perspectives.Frontiers in pharmacology · 2026Review
- Oxidative Stress and Antioxidants in Glioblastoma: Mechanisms of Action, Therapeutic Effects and Future Directions.Antioxidants (Basel, Switzerland) · 2025Review
- USP7 promotes temozolomide resistance by stabilizing MGMT in glioblastoma.Cell death & disease · 2025Article
- Awake brain MRSI reveals anesthetic sensitivity and regional aging effects on [Frontiers in neuroimaging · 2025Article
- Targeting Mitochondria in Glioma: New Hopes for a Cure.Biomedicines · 2024Review
- Mitochondrial Dysfunction: Effects and Therapeutic Implications in Cerebral Gliomas.Medicina (Kaunas, Lithuania) · 2024Review
- Ecto-NOX Disulfide-Thiol Exchanger 2 (ENOX2/tNOX) Is a Potential Prognostic Marker in Primary Malignant Melanoma and May Serve as a Therapeutic Target.International journal of molecular sciences · 2024Article
- Article
- Transcriptome Analysis Reveals Distinct Patterns Between the Invasive and Noninvasive Pituitary Neuroendocrine Tumors.Journal of the Endocrine Society · 2024Article
- Tolerable treatment of glioblastoma with redox-cycling 'mitocans': a comparative study in vivo.Redox report : communications in free radical research · 2023Article
- Article
- Redox-Cycling "Mitocans" as Effective New Developments in Anticancer Therapy.International journal of molecular sciences · 2023Article
- Menadione Potentiates Auranofin-Induced Glioblastoma Cell Death.International journal of molecular sciences · 2022Article
- Article
- Combination of Ascorbic Acid and Menadione Induces Cytotoxic Autophagy in Human Glioblastoma Cells.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Glioblastoma is one of the most aggressive brain tumors, characterized by a pronounced redox imbalance, expressed in a high oxidative capacity of cancer cells due to their elevated glycolytic and mitochondrial oxidative metabolism. The assessment and modulation of the redox state of glioblastoma are crucial factors that can provide highly specific targeting and treatment. Our study describes a pharmacological strategy for targeting glioblastoma using a redox-active combination drug. The experiments were conducted in vivo on glioblastoma mice (intracranial model) and in vitro on cell lines (cancer and normal) treated with the redox cycling pair menadione/ascorbate (M/A). The following parameters were analyzed in vivo using MRI or ex vivo on tissue and blood specimens: tumor growth, survival, cerebral perfusion, cellular density, tissue redox state, expression of tumor-associated NADH oxidase (tNOX) and transforming growth factor-beta 1 (TGF-β1). Dose-dependent effects of M/A on cell viability, mitochondrial functionality, and redox homeostasis were evaluated in vitro. M/A treatment suppressed tumor growth and significantly increased survival without adverse side effects. This was accompanied by increased oxidative stress, decreased reducing capacity, and decreased cellular density in the tumor only, as well as increased cerebral perfusion and down-regulation of tNOX and TGF-β1. M/A induced selective cytotoxicity and overproduction of mitochondrial superoxide in isolated glioblastoma cells, but not in normal microglial cells. This was accompanied by a significant decrease in the over-reduced state of cancer cells and impairment of their "pro-oncogenic" functionality, assessed by dose-dependent decreases in: NADH, NAD
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.