University of Würzburg Researchers Link Vitamin B2 Metabolism to Cancer Cell Resistance Against Ferroptosis

University of Würzburg researchers discover that vitamin B2 metabolism protects cancer cells from ferroptosis. Read how roseoflavin could trigger tumor death.

By: AXL Media

Published: Mar 14, 2026, 11:03 AM EDT

Source: Information for this article was sourced from University of Würzburg

The Dual Role of Riboflavin in Cellular Protection

Vitamin B2, commonly known as riboflavin, is an essential nutrient that the human body must acquire through dietary sources such as dairy, eggs, and green vegetables. While its primary role is to convert into molecules that protect healthy cells from oxidative damage, researchers at the Rudolf Virchow Centre at Julius-Maximilians-Universität Würzburg have discovered a significant medical downside. This protective function is actively hijacked by cancer cells to bolster their defenses against programmed cell death, specifically a unique iron-driven process known as ferroptosis.

Understanding the Mechanism of Ferroptosis

Ferroptosis is a distinct form of controlled cell death characterized by iron-dependent lipid peroxidation. Unlike other cellular suicide pathways, it occurs when a cell's antioxidant defenses are overwhelmed by oxidative stress. Because ferroptosis does not trigger the inflammation typically associated with tissue damage, it is a primary target for oncological research. The Würzburg study, published in Nature Cell Biology, highlights how vitamin B2 acts as a specialized cofactor that allows cancer cells to evade this death pathway, thereby maintaining tumor stability and growth.

The Role of FSP1 and Vitamin B2 Interaction

At the center of this metabolic defense is a protein known as FSP1, which is responsible for shielding cells from oxidative destruction. The research team, led by Professor José Pedro Friedmann Angeli, utilized genome editing to observe the interaction between riboflavin-derived cofactors and this protective protein. They discovered that when vitamin B2 is deficient or its metabolism is disrupted, the FSP1 protein loses its efficacy, leaving the cancer cells significantly more vulnerable to ferroptosis. This suggests that the vitamin B2 metabolic pathway is a primary vulnerability in a tumor's redox defense system.