|Higher standardized uptake value (SUV) in the livers of mice lacking|
TRAP-1 (right) indicates increased glucose consumption as a result
When TRAP-1 function was removed from cancer cells, the response was a catastrophic, causing metabolic problems that ultimately led to cell death. That's because cancer cells have very high energy needs, and the compensatory metabolic pathways were unable to meet the increased energy demands. Because TRAP-1 is important in both protecting cells and in oxidative phosphorylation, which is being increasingly recognized as a key ingredient in tumor proliferation, this protein has become an attractive therapeutic target in cancer cells. What is especially promising about this study is that the adverse effect of removing TRAP-1 function only occurred in cancer cells - it seemed to have a protective effect in healthy cells.
A few weeks ago, I wrote about a very interesting use of evolutionary game theory to figure out when cancer cells are most vulnerable - which is during the switch in energy production. What I find most remarkable about this study is that it provides a way to put this mathematical modeling into practice. When TRAP-1 function is removed, cancer cells become more vulnerable to apoptosis. Perhaps the key to fighting cancer may lie in the combination of both methods - in targeting TRAP-1 during critical transitions in cancer metabolisms to ensure efficient and effective treatment. While the problem remains finding the therapeutic windows for cancer vulnerability, the authors have definitely strengthened the case for targeting the Hsp90 family in the development of cancer therapies. They have also opened up a fascinating discussion on the implications of chaperone proteins in cellular metabolism and longevity.