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Flow Cytometric Measurement Of ROS Production In Macrophages In Response To FcγR Cross-linking
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ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling
Menghao Qiao1, Liqun Zhou1, Minhua Zhou1
1Key Laboratory of Regenerative Medicine of Ministry of Education, Institute of Aging and Regenerative Medicine, Department of Developmental & Regenerative Medicine, College of Life Science and Technology, Jinan University, Guangzhou, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|January 27, 2026
Summary
Ezrin, Radixin, and Moesin (ERM) proteins regulate ferroptosis, a form of cell death. Inhibiting ERM phosphorylation protects cells by modulating reactive oxygen species (ROS) and activating the NRF2 antioxidant pathway.
Area of Science:
- Cell Biology
- Biochemistry
- Oncology
Background:
- Ferroptosis is an iron-dependent cell death pathway crucial for cellular redox homeostasis.
- Ezrin, Radixin, and Moesin (ERM) proteins are known regulators of the membrane-actin cytoskeleton.
- The role of ERM proteins in ferroptosis has not been previously investigated.
Purpose of the Study:
- To investigate the role of ERM proteins in regulating ferroptosis.
- To elucidate the molecular mechanisms by which ERM proteins influence ferroptosis.
- To identify potential therapeutic targets for modulating ferroptosis.
Main Methods:
- Utilized human fibrosarcoma HT-1080 cells.
- Employed pharmacological inhibition of ERM phosphorylation, gene knockdown, and overexpression of Ezrin mutants.
- Assessed ferroptosis, reactive oxygen species (ROS) levels, F-actin dynamics, and NRF2 pathway activation.
Main Results:
- ERM protein inhibition or phosphorylation deficiency attenuated erastin-induced ferroptosis.
- ERM inhibition led to F-actin depolymerization and a rise in ROS, which was mitigated by F-actin stabilization.
- ROS elevation activated the KEAP1-NRF2 pathway, inducing antioxidant genes like HMOX1, conferring ferroptosis resistance.
Conclusions:
- ERM proteins are identified as novel modulators of ferroptosis.
- ERM inhibition confers resistance to ferroptosis via ROS-NRF2-mediated redox adaptation.
- ERM proteins represent a potential therapeutic target for diseases involving ferroptosis.
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