Cancer Vulnerability Discovered in Vitamin B7-Dependent Enzyme
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Researchers have identified a biological mechanism that exposes a vulnerability in tumor cells when they are deprived of vitamin B7 (biotin). The study reveals that a mitochondrial enzyme, pyruvate carboxylase, which requires biotin to function, is crucial for cancer cells to adapt when their primary nutrient, glutamine, is scarce. This finding explains why some therapies targeting glutamine fail and points to a potential new therapeutic strategy.
Facts First
- Tumor cells become vulnerable when deprived of vitamin B7 (biotin) due to the failure of a key mitochondrial enzyme.
- The enzyme pyruvate carboxylase requires biotin to function and allows cells to use pyruvate to grow when glutamine is scarce.
- Mutations in the FBXW7 gene can trigger increased glutamine dependence by reducing pyruvate carboxylase levels.
- The discovery explains why glutamine-blocking therapies sometimes fail, as cancer cells can switch to alternative metabolic pathways.
- The research was a collaboration between the University of Lausanne and Northeastern University in the United States.
What Happened
Researchers at the University of Lausanne (Unil) discovered a biological mechanism that exposes a vulnerability in tumor cells when they are deprived of vitamin B7 (biotin). The study, published in the journal Molecular Cell, was led by Dr. Miriam Lisci, a postdoctoral scientist in Prof. Alexis Jourdain's lab at Unil's Faculty of Biology and Medicine (FBM). The research focused on how cancer cells adapt when deprived of glutamine, a nutrient many tumors are heavily dependent on. The team found that cells can use pyruvate to continue dividing when glutamine is scarce, but this process depends on the mitochondrial enzyme pyruvate carboxylase, which requires biotin to function. Without biotin, the enzyme stops working and cell growth halts. The study also identified a role for the FBXW7 gene, showing that specific mutations found in patients can trigger increased dependence on glutamine by reducing pyruvate carboxylase levels.
Why this Matters to You
This discovery could lead to new strategies for treating cancer. If future therapies can exploit this newly identified vulnerability by targeting the biotin-dependent enzyme, they might be able to halt the growth of tumors that have become resistant to other treatments. For patients, this research may eventually translate into more effective and targeted treatment options, particularly for cancers driven by specific genetic mutations like those in the FBXW7 gene.
What's Next
The research team collaborated with metabolomics and proteomics platforms at FBM and a team at Northeastern University in the United States. This foundational discovery will likely lead to further research to... explore potential drug candidates that could block this specific metabolic pathway in cancer cells.