Researchers discover molecular pathway that mediates cancer-associated muscle atrophy

Nearly half of all cancer patients suffer from excessive weight loss due to the loss of adipose and skeletal muscle tissues, or cachexia. This progressive illness not only impairs quality of life for cancer patients but also poses a serious threat for treatment since it obstructs the use of effective medicines especially in advanced stages. Current research yet fails to offer an effective therapy to slow down or block this wasting because the driving forces behind the atrophy process remain incompletely understood.

A recent article published in Nature however, reveals an important molecular mechanism that can make a change in this process. The research led by Dr. Serkan Kır from Koç University in Istanbul, illustrates how the activation of EDA2R signaling promotes skeletal muscle atrophy and how the deletion of either EDA2R or the enzyme NIK, can be an effective way to protect the organism from muscle loss. In the article along with Şevval Nur Bilgiç and Aylin Domaniku, Dr. Serkan Kır identifies these novel molecular targets for anti-cachexia therapy.

Dr. Serkan Kır's laboratory at the Department of Molecular Biology and Genetics in Koç University utilizes molecular biology approaches, primary cell culture techniques, mouse tumor models and human tissue samples to dissect molecular mechanisms behind tumor signaling to adipose and muscle tissues.

With their recent article, "EDA2R–NIK signaling promotes muscle atrophy linked to cancer cachexia", the researchers arrived at a conclusion that targeting the these pathways may be a potential solution in preventing muscle loss. The fact that the activities of the components of this molecular pathway can be altered by drug usage indicates a strong potential for treatment.

The research team believes that this newly discovered molecular pathway could also play a role in complications leading to muscle loss beyond cachexia. Treatments for muscular dystrophy diseases and age-related muscle loss (sarcopenia) could also benefit from these findings. In their subsequent studies, the team plans to explore the roles of the relevant protein targets in other muscle loss disorders.