The vitamin B2 (riboflavin) must be absorbed through diet: it can be found in dairy products, eggs, meat, and green vegetables. The body’s metabolism converts vitamin B2 into molecules that protect the cell from oxidative damage. Now, a CRISPR–Cas9 screen has uncovered vitamin B2 as a modulator of ferroptosis sensitivity: it supports the stability of ferroptosis suppressor protein 1 (FSP1) and the recycling of lipid-soluble antioxidants, thereby mitigating phospholipid peroxidation. One outcome of this process may be that vitamin B2 also protects cancer cells. “Vitamin B2 plays a crucial role in protecting cancer cells from ferroptosis, a special form of programmed cell death,” said Vera Skafar, a PhD student who is a member of the research group led by José Pedro Friedmann Angeli, PhD, professor of translational cell biology at the Rudolf Virchow Centre (RVZ) at Julius-Maximilians-Universität Würzburg (JMU). This work is published in Nature Cell Biology in the paper, “Riboflavin metabolism shapes FSP1-driven ferroptosis resistance.” The body uses programmed cell death to allow damaged or dangerous cells to die in a controlled manner without causing inflammation in the surrounding tissue. Specifically, ferroptosis is associated with many pathological conditions, including cancer and neurodegeneration. Unlike other cell-death pathways, ferroptosis is triggered when iron-driven lipid peroxidation overwhelms a cell’s antioxidant protection. Cancer cells often evade ferroptosis by boosting redox defense systems. This study highlights vitamin B2 metabolism as an important contributor to those defenses, implying that targeting riboflavin-derived cofactors could weaken ferroptosis resistance and make tumors more vulnerable. The protein FSP1 is…
