ArticleCNS neuroscience & therapeutics2023
FHOD1 is upregulated in glioma cells and attenuates ferroptosis of glioma cells by targeting HSPB1 signaling.
Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Nanomagnetic Hyperthermia Sensitizes Gemcitabine Chemosensitivity in Pancreatic Cancer by Inhibiting HSPB1 to Amplify ACSL4-Mediated Ferroptosis.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Radiotherapy combined with anti-PD-1 immunotherapy promotes ferroptosis-driven control of hepatocellular carcinoma.Genes and immunity · 2026Article
- Global research landscape and hotspots for ferroptosis in glioma: A comprehensive bibliometric and visual analysis.Heliyon · 2025Review
- Role of FHOD1 in tumor cells and tumor immune microenvironment.Frontiers in immunology · 2025Review
- HSPB1 silencing enhances ferroptosis in glioma cells by suppressing BAG3 expression.American journal of translational research · 2025Article
- Exploration of the Prognostic Role of Apoptosis-Related Genes in Glioblastoma.Stem cells international · 2025Article
- FHOD1 is upregulated in glioma cells and attenuates ferroptosis of glioma cells by targeting HSPB1 signaling.CNS neuroscience & therapeutics · 2023Article
- CircRNF10 triggers a positive feedback loop to facilitate progression of glioblastoma via redeploying the ferroptosis defense in GSCs.Journal of experimental & clinical cancer research : CR · 2023Article
- GPX8 regulates pan-apoptosis in gliomas to promote microglial migration and mediate immunotherapy responses.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs a new type of regulatory cell death, ferroptosis has been proven to be involved in cancer pathogenesis and therapeutic response. However, the detailed roles of ferroptosis or ferroptosis-associated genes in glioma remain to be clarified.
methodsHere, we performed the TMT/iTRAQ-Based Quantitative Proteomic Approach to identify the differentially expressed proteins between glioma specimens and adjacent tissues. Kaplan-Meier survival was used to estimate the survival values. We also explored the regulatory roles of abnormally expressed formin homology 2 domain-containing protein 1 (FHOD1) in glioma ferroptosis sensitivity.
resultsIn our study, FHOD1 was identified to be the most significantly upregulated protein in glioma tissues. Multiple glioma datasets revealed that the glioma patients with low FHOD1 expression displayed favorable survival time. Functional analysis proved that the knockdown of FHOD1 inhibited cell growth and improved the cellular sensitivity to ferroptosis in glioma cells T98G and U251. Mechanically, we found the up-regulation and hypomethylation of HSPB1, a negative regulator of ferroptosis, in glioma tissues. FHOD1 knockdown could enhance the ferroptosis sensitivity of glioma cells via up-regulating the methylated heat-shock protein B (HSPB1). Overexpression of HSPB1 significantly reversed FHOD1 knockdown-mediated ferroptosis.
conclusionsIn summary, this study demonstrated that the FHOD1-HSPB1 axis exerts marked regulatory effects on ferroptosis, and might affect the prognosis and therapeutic response in glioma.
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