Protein imbalance in the development of skeletal muscle wasting in tumour‐bearing mice

Abstract

Our findings work towards understanding the pathophysiological signalling in skeletal muscle in the initial development of cancer cachexia. Shortly following the onset of the tumour-bearing state alterations in myogenic regulatory factors are apparent, suggesting early onset alterations in the capacity for myogenic induction. Cancer cachexia presents with a combination of a loss of protein synthesis and increased markers of protein breakdown, specifically in the ubiquitin-proteasome system. Also, p38 MAPK may be a potential therapeutic target to combat cancer cachexia via a p38-FOX01-atrogene-ubiquitin-proteasome mechanism.