ArticleBiochemistry and biophysics reports2025
Sorafenib induces ferroptosis in human renal cell carcinoma cells through CCAT/enhancer-binding protein homologous protein.
Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Translating the Crosstalk Between Unfolded Protein Response and Ferroptosis to Cancer Therapies.Current oncology reports · 2026Review
- GSH-Related Enzymes GPx4, Chac1, and GSTs and Redox Regulation of Ferroptosis in Cancer.International journal of molecular sciences · 2026Review
- Global evolution of ferroptosis research: a comprehensive bibliometric analysis of publication trends, geographic patterns, pharmacological innovation, and translational progress from inception through 2025.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Research progress on the regulation of ferroptosis in NPC (Review).Oncology reports · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Sorafenib, a multi-kinase inhibitor, has been shown to induce ferroptosis, a form of lipid peroxidation-mediated cell death. However, a mechanism of how sorafenib-induced ER stress leads to ferroptosis remains unclear. Here, we report that the CCAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) is a critical mediator linking ER stress to ferroptosis in human renal cell carcinoma (RCC) cells after exposure to sorafenib. A large portion of sorafenib-induced cell death was shown to be caused by ferroptosis and ER stress significantly contributed to this ferroptic cell death. Among three major ER stress pathways, sorafenib specifically induced activation of the ATF4-CHOP axis. CHOP in turn functioned as an effector suppressing expression of SLC7A11. Therefore, our results suggest that sorafenib induces ferroptosis in RCC cells by increasing uncontrolled oxidative stress.
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