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 reduces 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. There is no effective therapy to slow down or block this wasting because the driving forces behind the atrophy process are not 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 Serkan Kır from Koç University in Istanbul, Turkey, shows 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. The researchers said they have identified the novel molecular targets for anti-cachexia therapy.
Kır’s laboratory at the Department of Molecular Biology and Genetics in Koç University utilized 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.
Preventing muscle loss
The researchers said that targeting 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.
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