Mice Lacking a Specific Protein Live Longer, Study Finds
In a new study, researchers were using mice models to develop a new cancer drug when they discovered a link between the mice's lifespan and a particular protein. The team from the Wistar Institute reported that mice lacking a protein were more likely to live longer with fewer age-related diseases in comparison to mice that have the protein.
According to the researchers, the protein, TRAP-1, is responsible for regulating metabolism and energy production in the mitochondria if the cells are healthy. In cancer cells, TRAP-1 becomes overproduced, which negatively affects the amount of energy that the mitochondria produce.
"In tumors, the loss of TRAP-1 is devastating, triggering a host of catastrophic defects, including metabolic problems that ultimately result in in death of the tumor cells," Dario C. Altieri, M.D., Robert and Penny Fox Distinguished Professor and director of The Wistar Institute's National Cancer Institute-designated Cancer Center, said.
In this study, the researchers genetically altered mice to lack the TRAP-1 protein. Without this protein, the mitochondria do not make enough energy for the cells. The researchers found that this group of mice, called the "knockout" mice, was capable of using other cellular mechanisms to make energy. The team found that not only could the knockout mice compensate for the loss of energy, they also had less tissue degeneration tied to aging. The knockout mice also lived longer, had a lower risk of obesity and demonstrated spontaneous tumor formation.
"We see this astounding change in TRAP-1 knockout mice, where they show fewer signs of aging and are less likely to develop cancers," said Altieri reported in the press release. "Our findings provide an unexpected explanation for how TRAP-1 and related proteins regulate metabolism within our cells. We usually link the reprogramming of metabolic pathways with human diseases, such as cancer. What we didn't expect to see were healthier mice with fewer tumors."
The study was published in the journal, Cell Reports.