When cancer cells face starvation, they have an escape route — and researchers just found the key to locking it shut. Scientists at the University of Lausanne have discovered that vitamin B7, commonly known as biotin, acts as a kind of "metabolic license" that allows cancer cells to survive when nutrient supplies run low. Block that license, and tumors may lose their survival strategy.
The research, published in the journal Molecular Cell, was led by Dr. Miriam Lisci, a postdoctoral scientist in the lab of Alexis Jourdain, assistant professor in the Department of Immunobiology at the Faculty of Biology and Medicine. Their work centers on how cancer cells adapt when their preferred fuel source — the amino acid glutamine — becomes scarce. Many tumors are what scientists call "glutamine addicted," relying heavily on this nutrient to build proteins and DNA. But when glutamine runs out, some cancers find a workaround: they switch to an alternative fuel source called pyruvate.
This switch depends on an enzyme called pyruvate carboxylase, which requires biotin to function. "When vitamin B7 is not available, the enzyme stops working, and cell growth comes to a halt," the researchers found. In other words, biotin gives cells permission to tap into pyruvate as a backup energy source — hence the "metabolic license" analogy.
The study also revealed a critical vulnerability linked to a gene called FBXW7, which is frequently mutated in certain cancers. "When FBXW7 is mutated, pyruvate carboxylase partially disappears, pyruvate can no longer be used efficiently, and cells become dependent on glutamine," explained Dr. Lisci, first author of the paper. This means tumors with FBXW7 mutations lose their backup route and become even more dependent on glutamine — potentially making them easier to starve.
The findings help explain why some therapies targeting glutamine metabolism fail. Cancer cells are metabolic survivors; when one pathway closes, they reroute through another. But by exposing the biotin-dependent mechanism behind this flexibility, the Lausanne team has identified a new angle of attack.
"In the longer term, this research opens up new avenues for better understanding the metabolic vulnerabilities of cancers and for designing innovative therapeutic strategies that take into account the great metabolic flexibility of tumor cells, notably by targeting several metabolic pathways simultaneously," said Professor Jourdain. The research was conducted in collaboration with teams at Northeastern University in the United States, along with the faculty's metabolomics and proteomics platforms.
The road from laboratory discovery to patient treatment is long, but these findings offer a promising new direction: instead of trying to block just one metabolic route, future treatments might cut off several at once, leaving cancer cells with nowhere left to run.