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Tamarixetin induces ferroptotic stress through the SLC7A11–GPX4 axis and triggers a compensatory NRF2 response

GSE327198 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/05/11 Platform GPL30173
Summary
Ferroptosis has emerged as a therapeutic vulnerability in hepatocellular carcinoma, but its interplay with antioxidant defense remains incompletely understood. Here, we investigated whether Tamarixetin induces ferroptotic stress in hepatoma cells and how nuclear factor erythroid 2-related factor 2 (NRF2) signaling responds to this process. Tamarixetin selectively reduced hepatoma cell viability, increased lipid peroxidation, and these effects were partially rescued by ferrostatin-1. Transcriptome analysis revealed enrichment of ferroptosis- and glutathione metabolism-related pathways, highlighting redox-associated genes centered on the SLC7A11–glutathione peroxidase 4 (GPX4) axis. Tamarixetin also increased NRF2 target gene expression, indicating activation of a compensatory antioxidant response to oxidative stress. Molecular docking further suggested a potential interaction between Tamarixetin and the xCT transporter. These findings identify Tamarixetin as a modulator of ferroptotic stress in hepatoma cells and support redox-targeting strategies for liver cancer.
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Also filed as BioProject PRJNA1449946 and SRA study SRP689820. Searching any of these in the dataset finder brings you back here.

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