Researchers at the University of Lausanne in Switzerland have discovered that a deficiency of vitamin B7 blocks alternative energy pathways in cancer cells, thereby inhibiting their growth. This study, published in the journal Molecular Cell, reveals new insights into how the metabolic flexibility of cancer cells can be diminished. Malfunction in the gene FBXW7 forces cancer cells to rely solely on glutamine, making drugs that inhibit glutamine potentially more effective. Kathmandu, 7 Baisakh.
Scientists have achieved a significant breakthrough in cancer treatment. According to researchers from the University of Lausanne, the lack of vitamin B7 (biotin) prevents cancer cells from activating alternative energy pathways, effectively halting their proliferation. This new finding published in Molecular Cell sheds light on ways to reduce the metabolic adaptability of cancer cells.
Typically, many cancer cells depend heavily on the amino acid glutamine, a phenomenon known as “glutamine addiction.” When glutamine supply is cut off during cancer therapy, these cells often survive and continue to grow by utilizing other nutrients such as pyruvate as fuel. For this alternative metabolic route, cancer cells require activation of the enzyme pyruvate carboxylase, which necessitates vitamin B7.
The study shows that in the absence of vitamin B7, pyruvate carboxylase activity ceases, preventing cancer cells from accessing alternative energy sources, which leads to cell death. This investigation also elucidated the role of the gene FBXW7, which is frequently mutated in many cancer patients. Mutation in this gene reduces pyruvate enzyme levels, rendering cancer cells entirely dependent on glutamine. In such cases, drugs that inhibit glutamine metabolism are likely to be more effective. This discovery not only explains why some cancer drugs fail in certain cases but also paves the way for developing new and targeted treatments aimed at exploiting metabolic vulnerabilities in cancer cells.
