Related Experiment Video

Updated: Mar 15, 2026

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

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Riboflavin metabolism shapes FSP1-driven ferroptosis resistance

Vera Skafar1, Izadora de Souza1, Biplab Ghosh2,3

  • 1Rudolf Virchow Zentrum (RVZ), Center for Integrative and Translational Bioimaging, University of Würzburg, Würzburg, Germany.

Nature Cell Biology
|March 14, 2026
PubMed

Insights

Riboflavin (vitamin B2) supports ferroptosis suppressor protein 1 (FSP1) function, protecting cells from oxidative damage. Targeting riboflavin metabolism offers a new strategy against ferroptosis in cancer.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Nutritional Science

Background:

  • Cellular membrane protection relies on antioxidants like GPX4, ubiquinone, and vitamin E.
  • Ferroptosis suppressor protein 1 (FSP1) inhibits ferroptosis by regenerating membrane antioxidants.
  • Regulators of FSP1 are largely unknown, hindering understanding of ferroptosis buffering mechanisms.

Purpose of the Study:

  • To identify novel regulators of ferroptosis suppressor protein 1 (FSP1) function.
  • To investigate the role of identified factors in cellular antioxidant capacity and ferroptosis sensitivity.
  • To explore therapeutic strategies targeting FSP1-mediated antioxidant recycling.

Main Methods:

  • Utilized a CRISPR-Cas9 screening approach to identify FSP1 regulators.
  • Investigated the impact of riboflavin and its antimetabolite roseoflavin on FSP1 activity.
  • Assessed cellular sensitivity to ferroptosis under varying nutrient conditions.

Main Results:

  • Identified riboflavin (vitamin B2) as a key modulator of ferroptosis sensitivity.
  • Demonstrated that riboflavin enhances FSP1 stability and antioxidant recycling.
  • Showed that roseoflavin impairs FSP1 function, increasing cancer cell susceptibility to ferroptosis.

Conclusions:

  • Riboflavin is crucial for maintaining FSP1-dependent antioxidant defense.
  • Targeting riboflavin metabolism presents a potential therapeutic avenue for ferroptosis-related diseases, including cancer.
  • This study highlights the interplay between nutrients and cellular antioxidant systems.

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