Biotin lets cancer cells escape glutamine dependence, study shows
Mar 2nd 2026
A Molecular Cell study led by Alexis Jourdain shows biotin activates pyruvate carboxylase so pyruvate can compensate for glutamine loss, while FBXW7 mutations block this switch and create glutamine addiction, with implications for cancer treatment.
- Biotin (vitamin B7) is required for pyruvate carboxylase to function and lets cells grow without glutamine.
- Pyruvate can replace glutamine by fueling the TCA cycle when pyruvate carboxylase is active.
- Mutations in the FBXW7 gene lower pyruvate carboxylase levels and make cancer cells dependent on glutamine.
- Some FBXW7 mutations found in patients directly cause this metabolic addiction.
- The work helps explain failures of glutamine-targeting therapies and supports testing combined metabolic-targeting strategies.