ArticleNature communications2021
Suppression of mitochondrial ROS by prohibitin drives glioblastoma progression and therapeutic resistance.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 135 citations in OpenAlex.
- SQOR regulates HResearch square · 2026Article
- Tumor microenvironment-responsive nanocarriers for enhanced glioblastoma immunotherapy.Journal of nanobiotechnology · 2026Review
- Host-directed antiviral strategy targeting prohibitins: Mel56 suppresses influenza A virus and severe acute respiratory syndrome coronavirus 2 via modulation of antioxidant pathways and mitochondrial function.Microbiology spectrum · 2026Article
- Fungal oxidative stress tolerance depends on peroxiredoxin PrxA-mediated redox signaling to mitochondrial cytochrome c peroxidase Ccp1.The Journal of biological chemistry · 2026Article
- Cancer stem cells synthesize proline to attenuate oxidative stress.The Journal of clinical investigation · 2026Article
- Thr3/Ser90 phosphorylation-stabilized S100A8 regulates cholesterol metabolism in glioblastoma stem cells.Oncogene · 2026Article
- ITPR1 Maintains Mitochondrial Redox Homeostasis to Drive Glioblastoma Progression Through Recruitment and Activation of DRP1.Antioxidants (Basel, Switzerland) · 2026Article
- Dual suppression of stemness and redox adaptation in glioblastoma through filaggrin upregulation by an abiraterone-based HDAC inhibitor.Journal of biomedical science · 2026Article
- Inhibition of IRE1α kinase increases ferroptosis resistance in triple-negative breast cancer cells.Oncology letters · 2026Article
- A Mussel-Inspired Bioadhesive Patch to Selectively Kill Glioblastoma Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Glioblastoma cells that evade chemoradiotherapy-induced cell death exhibit a bifurcated glycolytic program.Cell death & disease · 2026Article
- The Redox Properties of Polyphenols and Their Role in ROS Generation for Biomedical Applications.Angewandte Chemie (International ed. in English) · 2026Review
- Cancer stem cell programs S-nitrosylation and deubiquitination of FoxP3 protein to promote regulatory T cell differentiation.Frontiers in immunology · 2026Article
- Mapping the global research landscape and innovations on elderly glioma: a bibliometric analysis.Frontiers in oncology · 2026Article
- Crosstalk in the brain tumor microenvironment: mechanisms, therapeutic strategies, and clinical advances.Military Medical Research · 2026Review
- Identification of the Antioxidant Enzyme B166 as a Novel Biomarker for Patients With Glioblastoma Multiforme.Analytical cellular pathology (Amsterdam) · 2026Article
- Propofol and Glioblastoma Biology: A Narrative Review of Perioperative Clinical Evidence and PI3K/AKT-Wnt-miRNA, GABA-A, and Immune-Checkpoint Pathways.BioMed research international · 2026Review
- CYBC1 Drives Glioblastoma Progression via Reactive Oxygen Species and NF-κB Pathways.Cancer research and treatment · 2025Article
- BLVRA promotes glioblastoma progression by regulating fatty acid metabolism.Scientific reports · 2025Article
- Targeting the Mitochondria in High-Grade Gliomas.Cancers · 2025Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low levels of reactive oxygen species (ROS) are crucial for maintaining cancer stem cells (CSCs) and their ability to resist therapy, but the ROS regulatory mechanisms in CSCs remains to be explored. Here, we discover that prohibitin (PHB) specifically regulates mitochondrial ROS production in glioma stem-like cells (GSCs) and facilitates GSC radiotherapeutic resistance. We find that PHB is upregulated in GSCs and is associated with malignant gliomas progression and poor prognosis. PHB binds to peroxiredoxin3 (PRDX3), a mitochondrion-specific peroxidase, and stabilizes PRDX3 protein through the ubiquitin-proteasome pathway. Knockout of PHB dramatically elevates ROS levels, thereby inhibiting GSC self-renewal. Importantly, deletion or pharmacological inhibition of PHB potently slows tumor growth and sensitizes tumors to radiotherapy, thus providing significant survival benefits in GSC-derived orthotopic tumors and glioblastoma patient-derived xenografts. These results reveal a selective role of PHB in mitochondrial ROS regulation in GSCs and suggest that targeting PHB improves radiotherapeutic efficacy in glioblastoma.
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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.