ArticleCell death & disease2025
Transcriptional activation of PHKG2 by TP53 promotes ferroptosis through nuclear export of NRF2 in head and neck squamous cell carcinoma.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Bacterial extracellular vesicles from Streptococcus mutans drive OSCC progression through β-catenin signaling.Scientific reports · 2026Article
- TPI1 promotes malignant progression and ferroptosis resistance in head and neck squamous cell carcinoma.Frontiers in genetics · 2026Article
- Advances in ferroptosis mechanisms and therapeutic potential in head and neck squamous cell carcinoma.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
8 authors.
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Abstract
Head and neck squamous cell carcinoma (HNSCC) is a common malignancy with a poor prognosis despite multiple available treatments. Ferroptosis, an iron-dependent form of regulated cell death characterized by lipid peroxidation, has recently emerged as a promising strategy for cancer therapy, particularly in head and neck malignancies. However, its regulatory mechanisms remain largely unclear. In this study, we demonstrate that TP53 transcriptionally activates PHKG2, which promotes ferroptosis. PHKG2 enhances the activity of protein phosphatase 1 (PP1) by phosphorylating PPP1R3B, disrupting its interaction with PP1C. Activated PP1 dephosphorylates NRF2, promoting its nuclear export and suppressing GPX4 transcription, thereby enhancing ferroptosis sensitivity. Both in vitro and in vivo, PHKG2 overexpression significantly suppressed tumor growth and increased lipid peroxidation levels. These findings define a previously unrecognized TP53/PHKG2-PP1-NRF2 signaling axis in the regulation of ferroptosis in HNSCC and suggest a novel therapeutic target.
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