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| Wistar Institute |
According to researchers at the Wistar Institute in Philadelphia, mice that lack a specific regulator protein live longer than mice that have it, a finding that sheds light on how metabolic networks might play a role in cancer treatment, aging and obesity.
The TRAP-1 protein is a metabolism regulator that controls energy production in mitochondria. And in cancer cells TRAP-1 is overproduced, leading to faster multiplication. So in mice with the inability to produce this protein, fewer signs of aging appeared and the presence of tumors reduced, demonstrating that the metabolic processes were successfully dampened.
This can have a crucial impact on cancer cells, according to the team's study published in the journal Cell Reports.
"We usually link the reprogramming of metabolic pathways with human diseases, such as cancer," lead author Dario Altieri said in a statement. "What we didn't expect to see were healthier mice with fewer tumors."
In not having the TRAP-1 protein, the mice's mitochondrial proteins misfolded, causing the cells to work harder. This sped up the mice's metabolism and damaged DNA--not to a harmful extent--slowing the proliferation of tumors. The findings elucidate the mechanisms of "chaperone" proteins such as TRAP-1, included in the protein family HSP90.
"Our findings strengthen the case for targeting HSP90 in tumor cells, but they also open up a fascinating array of questions that may have implications for metabolism and longevity," Altieri said. "I predict that the TRAP-1 knockout mouse will be a valuable tool for answering these questions."
- here's the release