A vitamin we need to live is giving cancer cells some backup. New research suggests vitamin B2, also known as riboflavin, helps cancer cells protect themselves from ferroptosis, a type of programmed cell death.

The study, led by researchers at the University of Würzburg in Germany, found cancer cells became more vulnerable to ferroptosis when they were deprived of vitamin B2.

“Vitamin B2 plays a crucial role in protecting cancer cells from ferroptosis, a special form of programmed cell death,” biologist Vera Skafar, from the University of Würzburg, said.

The researchers found vitamin B2 helps a protein called FSP1, short for ferroptosis suppressor protein 1. Studies in recent years have shown FSP1 can protect cells from ferroptosis, alongside another protein called GPX4, or glutathione peroxidase 4.

After screening thousands of genes, the team found FSP1 depended on a gene called RFK, which is involved in processing vitamin B2 into forms the body can use. Further lab tests confirmed that vitamin B2 was fueling FSP1 through the RFK gene.

Those tests also pointed to a possible way to disrupt that protection. In lab-grown cancer cells, a vitamin B2 mimic called roseoflavin appeared to promote ferroptosis.

The researchers said roseoflavin seems to trick cancer cells into taking it up instead of vitamin B2, but it does not support FSP1 or the same cell defence in the way vitamin B2 does.

“This framework constitutes a previously underappreciated approach for enhancing ferroptosis in cancer cells and other contexts where FSP1 supports survival,” the researchers wrote in their paper.

The study does not suggest vitamin B2 is dangerous. The body does not produce it naturally and people need to get it from foods including dairy products, eggs, meat and green vegetables.

The researchers said the next step is to work out how to target this process specifically in cancer cells. They also noted ferroptosis is linked to other conditions beyond cancer.

“Ferroptosis is not only relevant to cancer,” biologist José Pedro Friedmann Angeli, from the University of Würzburg, said. “Increasing evidence suggests that it also contributes to pathological processes in neurodegenerative diseases and in tissue damage following organ transplantation or ischemia-reperfusion injury.”

The research was published in Nature Cell Biology.

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