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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
PubMed
Summary
This summary is machine-generated.

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.

Keywords:
ActinERM proteinsFerroptosisHMOX1NRF2ROS

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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.