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Approximately half of cancer patients experience excessive weight loss due to loss of adipose and skeletal muscle tissue or cachexia. This progressive disease not only impairs the quality of life of cancer patients, but also poses a serious threat to treatment as it hinders the use of effective medications especially in advanced stages. Current research has failed to provide an effective treatment to slow or prevent this wasting because the driving forces behind the atrophic process are still not fully understood.
A recent article published in the journal Nature reveals an important molecular mechanism that could alter this process. The research, led by Dr. Serkan Ker of Koç University in Istanbul, demonstrates how activation of EDA2R signaling promotes skeletal muscle atrophy and how deletion of EDA2R or the NIK enzyme could be an effective way to protect an organism from muscle loss. In the article with Evval Nur Bilgić and Aylin Domanico, Dr. Serkan Ker identifies these new molecular targets for anti-cachexia therapy.
Dr. Serkan Ker’s lab at the Department of Molecular Biology and Genetics at Koç University uses molecular biology approaches, primary cell culture techniques, mouse tumor models and human tissue samples to dissect the molecular mechanisms behind tumor signaling to adipose and muscle tissues.
With their recent article, “EDA2R–NIK signaling promotes muscle atrophy associated with cachexia,” the researchers came to the conclusion that targeting these pathways may be a potential solution in preventing muscle loss. The fact that the activities of components of this molecular pathway can be altered by drug administration indicates a strong potential for treatment.
The research team believes that this newly discovered molecular pathway could also play a role in the complications that lead to muscle loss after cachexia. Treatments for muscular dystrophy and age-related muscle loss (sarcopenia) could also benefit from these findings. In their subsequent studies, the team plans to explore the roles of relevant protein targets in other muscle loss disorders.
source:
Journal reference:
Belgic, S.N., et al. (2023) EDA2R–NIK signaling promotes muscular atrophy associated with cancerous cachexia. nature. doi.org/10.1038/s41586-023-06047-y.
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