ArticleRedox biology2024
A targetable PRR11-DHODH axis drives ferroptosis- and temozolomide-resistance in glioblastoma.
Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- A Selective Pro-Oxidant Drives Redox Reprogramming to Induce Ferroptosis and Immune Remodeling in Glioblastoma.Smart medicine · 2026Article
- DH-AUTAC induces ferroptosis in colorectal cancer by targeting DHODH for autophagic degradation through KCTD10-SQSTM1 signaling.Journal of gastroenterology · 2026Article
- A functional landscape for chromosome 17q in neuroblastoma: balancing replication stress and genomic stability.British journal of cancer · 2026Review
- DHODH-Mediated Suppression of Ferroptosis Supports Radioresistance and Represents a Therapeutic Vulnerability in Lung Cancer.Cancer research · 2026Article
- Stress granules restrain ferroptosis by sequestering ferritin.Nature cell biology · 2026Article
- CoQExperimental & molecular medicine · 2026Review
- Supramolecular self-assembled polyphenol nanoparticles alleviate osteoarthritis by inhibiting chondrocyte ferroptosis.Materials today. Bio · 2026Article
- H4K8 lactylation-mediated ferroptosis defense drives EGFR-TKI resistance in lung adenocarcinoma.Apoptosis : an international journal on programmed cell death · 2026Article
- Metabolic regulation of ferroptosis in cancer: mechanisms, pharmacological inducers, and translational challenges.Apoptosis : an international journal on programmed cell death · 2026Review
- PRR11 as a newly identified oncogenic driver in retinoblastoma.Science China. Life sciences · 2026Article
- ITPR1 Maintains Mitochondrial Redox Homeostasis to Drive Glioblastoma Progression Through Recruitment and Activation of DRP1.Antioxidants (Basel, Switzerland) · 2026Article
- GPR40 Attenuates Glioma TMZ-Resistance Through Ferroptosis Inhibition.Neurochemical research · 2026Article
- Targeting ferroptosis in cancer: from mechanistic insights to therapeutic approaches.Molecular biomedicine · 2026Review
- Unlocking glioma vulnerabilities: targeting regulated cell death pathways for innovative therapies.Cell death discovery · 2026Review
- Post-translational modifications in ferroptosis: mechanisms and therapeutic potential.International journal of biological sciences · 2026Review
- Bridging innate immunity and iron-dependent death: the interplay between cyclic GMP-AMP synthase-stimulator of interferon genes nexus and ferroptosis in cancer and inflammation.Frontiers in cell and developmental biology · 2026Review
- Targeting the NSUN2-DHODH axis reverses ferroptosis resistance and oxaliplatin resistance in colorectal cancer.Frontiers in pharmacology · 2026Article
- Review
- Rubidium chloride induces ferroptosis in glioblastoma cells by disrupting glutathione metabolism and redox homeostasis.Cancer cell international · 2025Article
- Harnessing ferroptosis to transform glioblastoma therapy and surmount treatment resistance.Cell death discovery · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Temozolomide (TMZ) is a widely utilized chemotherapy treatment for patients with glioblastoma (GBM), although drug resistance constitutes a major therapeutic hurdle. Emerging evidence suggests that ferroptosis-mediated therapy could offer an appropriate alternative treatment option against cancer cells that are resistant to certain drugs. However, recurrent gliomas display robust ferroptosis resistance, although the precise mechanism of resistance remains elusive. In the present work, we report that proline rich protein 11 (PRR11) depletion significantly sensitizes GBM cells to TMZ by inducing ferroptosis. Mechanistically, PRR11 directly binds to and stabilizes dihydroorotate dehydrogenase (DHODH), which leads to glioma ferroptosis-resistant in a DHODH-dependent manner in vivo and in vitro. Furthermore, PRR11 inhibits HERC4 and DHODH binding, by suppressing the recruitment of E3 ubiquitin ligase HERC4 and polyubiquitination degradation of DHODH at the K306 site, which maintains DHODH protein stability. Importantly, downregulated PRR11 increases lipid peroxidation and alters DHODH-mediated mitochondrial morphology, thereby promoting ferroptosis and increasing TMZ chemotherapy sensitivity. In conclusion, our results reveal a mechanism via which PRR11 drives ferroptosis resistance and identifies ferroptosis induction and TMZ as an attractive combined therapeutic strategy for GBM.
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