ArticleOncogenesis2022
Mitochondrial dysfunction and impaired growth of glioblastoma cell lines caused by antimicrobial agents inducing ferroptosis under glucose starvation.
Article in Oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Ferroptosis-induced oxidative stress in therapy-resistant glioblastoma.Cell death discovery · 2026Article
- FLASH Radiotherapy and Organelle-Targeted Radiosensitization in Glioblastoma: A Conceptual and Translational Review.Cancers · 2026Review
- Metabolic adaptations in cancer progression.Physiological reviews · 2026Review
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Demethoxycurcumin induces apoptosis and reduces cell migration by affecting AKT/mTOR-dependent autophagy in human glioma U87MG and T98G cell lines.Molecular biology reports · 2025Article
- Polysialylation of Glioblastoma Cells Is Regulated by Autophagy Under Nutrient Deprivation.International journal of molecular sciences · 2025Article
- MTFR1 phosphorylation-activated adaptive mitochondrial fusion is essential for colon cancer cell survival during glucose deprivation.Neoplasia (New York, N.Y.) · 2025Article
- Cardiolipin Dysregulation in Glioblastoma-Effects on Mitochondrial Function Tumor Cell Death and Sensitivity to Mitochondria-Targeting Drugs.Journal of cellular physiology · 2025Review
- Nrf2 and Ferroptosis: Exploring Translational Avenues for Therapeutic Approaches to Neurological Diseases.Current drug targets · 2025Review
- Glutaminolysis is associated with mitochondrial pathway activation and can be therapeutically targeted in glioblastoma.Cancer & metabolism · 2024Article
- Metabolic Contrasts: Fatty Acid Oxidation and Ketone Bodies in Healthy Brains vs. Glioblastoma Multiforme.International journal of molecular sciences · 2024Review
- Article
- VEGFR2 blockade inhibits glioblastoma cell proliferation by enhancing mitochondrial biogenesis.Journal of translational medicine · 2024Article
- Evaluation of the theranostic potential of [EJNMMI research · 2024Article
- Successful application of dietary ketogenic metabolic therapy in patients with glioblastoma: a clinical study.Frontiers in nutrition · 2024Article
- Improving lysosomal ferroptosis with NMN administration protects against heart failure.Life science alliance · 2023Article
- Induction of glioblastoma cell ferroptosis using combined treatment with chloramphenicol and 2-deoxy-D-glucose.Scientific reports · 2023Article
- Molecular mechanisms of ferroptosis and the potential therapeutic targets of ferroptosis signaling pathways for glioblastoma.Frontiers in pharmacology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma is a difficult-to-cure disease owing to its malignancy. Under normal circumstances, cancer is dependent on the glycolytic system for growth, and mitochondrial oxidative phosphorylation (OXPHOS) is not well utilized. Here, we investigated the efficacy of mitochondria-targeted glioblastoma therapy in cell lines including U87MG, LN229, U373, T98G, and two patient-derived stem-like cells. When glioblastoma cells were exposed to a glucose-starved condition (100 mg/l), they rely on mitochondrial OXPHOS for growth, and mitochondrial translation product production is enhanced. Under these circumstances, drugs that inhibit mitochondrial translation, called antimicrobial agents, can cause mitochondrial dysfunction and thus can serve as a therapeutic option for glioblastoma. Antimicrobial agents activated the nuclear factor erythroid 2-related factor 2-Kelch-like ECH-associated protein 1 pathway, resulting in increased expression of heme oxygenase-1. Accumulation of lipid peroxides resulted from the accumulation of divalent iron, and cell death occurred via ferroptosis. In conclusion, mitochondrial OXPHOS is upregulated in glioblastoma upon glucose starvation. Under this condition, antimicrobial agents cause cell death via ferroptosis. The findings hold promise for the treatment of glioblastoma.
Identifiers
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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.