Researchers at the Francis Crick Institute examined how restricting intake of vitamin B5 affects the growth of breast cancer cells. The findings, published in Nature Metabolism, highlight a link between vitamin B5 availability and cancer cell metabolism in both mouse models and human tissue samples.
The study began by showing that vitamin B5 is plentiful in many cancer cells and that these cells often exhibit high activity of the Myc gene, a driver of tumor growth. The heightened activity of Myc increased the production of a vitamin transport protein, enabling more vitamin B5 to enter cancer cells and potentially fueling their proliferation.
To test the blood sugar in the tumor environment, researchers fed mice diets with reduced vitamin B5. The tumors in these animals grew more slowly than those in mice on a standard diet. Parallel experiments with human breast cancer tissue in mice produced the same outcome, reinforcing the observation that limited dietary B5 can temper tumor expansion in this model.
Scientists propose that the observed effects stem from the conversion of vitamin B5 to coenzyme A inside cells. Coenzyme A participates in numerous metabolic pathways, supporting energy production and the synthesis of fats, carbohydrates, and proteins that collectively enable tumor cells to grow more effectively.
Despite these findings, the researchers caution that directly limiting vitamin B5 intake by cancer patients is not advised. A deficiency in vitamin B5 can compromise immune function, which is a key ally in fighting tumors. Ongoing efforts are focused on developing strategies to intercept vitamin B5 access by cancer cells while safeguarding immune defenses in the patient.
For context, accumulating evidence continues to shape the understanding of vitamin roles in cancer, underscoring the complexity of tumor metabolism and the careful balance required in nutritional guidance during cancer care. The Crick Institute team emphasizes that translating these observations to clinical practice will demand rigorous testing in humans and a clearer picture of how vitamin B5 interacts with other metabolic pathways and immune responses across different cancer types. The work contributes a piece to the broader effort to identify metabolic vulnerabilities in cancer cells that could be targeted without harming healthy tissue. Researchers suggest that future studies may explore selective blockade of vitamin B5 uptake by tumors or targeted modulation of downstream metabolic processes as possible therapeutic avenues, always with attention to preserving the patient’s immune function and overall health. [Citation: Francis Crick Institute study]