Patients diagnosed with p53-mutation cancers, such as soft-tissue sarcomas or cancers of the colon, lung, breast, liver, brain and hemopoietic tissues, may be able to improve muscle cellular health through exercise training, a study from York University finds.
Researchers in York University’s Muscle Health Research Centre investigated the role of the protein p53 in regulating mitochondria both basally and under the influence of exercise. Mitochondria are dynamic organelles that produce energy for the cell.
The protein p53 maintains normal mitochondrial content and function in muscle, but when mutated leads to reduced mitochondrial function and causes cancer. This research finds first evidence that muscle can still adapt to exercise in the absence of p53, and muscle mitochondrial benefits are still possible.
David Hood
“p53 is vital for cellular health, but when you exercise, at least some of the benefits of exercise do not rely on the presence of p53,” said David Hood, NSERC Tier 1 Canada Research Chair in Cell Physiology and director of York University’s Muscle Health Research Centre.
Furthering this line of research, said Hood, could be performed by determining the systemic benefit of exercise training on p53-mutated cancers in other organ systems and at the patient level in terms of symptom response.
“This would provide a valuable transition of our current work to assist physicians in incorporating a physical exercise model into the current plan of care to improve patient health,” he said.
The study, “The Role of p53 in Determining Mitochondrial Adaptations to Endurance Training in Skeletal Muscle,” was published Oct. 2 in Scientific Reports.