Muscle protein breakdown in cancer cachexia#br#

Zhang Ying; Wang Xinying

doi:10.16689/j.cnki.cn11－9349/r.2020.03.001

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Electronic Journal of Metabolism and Nutrition of Cancer ›› 2020, Vol. 7 ›› Issue (3) : 255-258. DOI: 10.16689/j.cnki.cn11－9349/r.2020.03.001

Muscle protein breakdown in cancer cachexia#br#

Zhang Ying1, Wang Xinying2

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Abstract

Muscle wasting is the central characteristic of cancer cachexia, which is associated with increased postoperative complication rates, increased susceptibility to chemotherapy toxicity, and decreased chance of survival. The muscle loss is caused by an imbalance between protein synthesis and degradation. In cancer patients, increased muscle protein breakdown seemed to play a more important role than decreased protein synthesis. The ubiquitin proteasome system (UPS) and autophagy lysosome system (ALS) are major intracellular proteolytic systems. UPS is the primary proteolytic route for short-lived, misfolded, and damaged proteins. It has important functions in the regulation of cell signaling and transcription and is involved in a variety of cellular functions, including cell cycle progression, cell survival, proliferation, apoptosis, and other critical cellular pathways. ALP recognizes and removes large and potentially dangerous cellular components such as protein aggregates and dysfunctional or superfluous organelles and has emerged as a crucial adaptive mechanism to cope with various cellular stresses. In the past, ubiquitin and the autophagy system were considered to be two independent systems. However, more and more studies show that they are closely related and functionally related systems,which serve complimentary roles in degrading cellular constituents and might be coordinately activated by common signaling mechanisms. In this review we will describe the involvement of the ubiquitin proteasome and autophagy lysosome systems in cancer cachexia that regulate tumor-induced protein breakdown in muscle.

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Zhang Ying, Wang Xinying. Muscle protein breakdown in cancer cachexia#br#[J]. Electronic Journal of Metabolism and Nutrition of Cancer. 2020, 7(3): 255-258 https://doi.org/10.16689/j.cnki.cn11－9349/r.2020.03.001

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