Cancer-associated
cachexia is a heterogeneous, multifactorial syndrome characterized by systemic
inflammation, unintentional
weight loss, and profound alteration in body composition. The main feature of
cancer cachexia is represented by the loss of skeletal muscle tissue, which may or may not be accompanied by significant adipose tissue wasting. Such phenotypic alteration occurs as the result of concomitant increased myofibril breakdown and reduced
muscle protein synthesis, actively contributing to
fatigue, worsening of quality of life, and refractoriness to
chemotherapy. According to the classical view, this condition is primarily triggered by interactions between specific
tumor-induced pro-inflammatory
cytokines and their cognate receptors expressed on the myocyte membrane. This causes a shift in gene expression of muscle cells, eventually leading to a pronounced catabolic condition and cell death. More recent studies, however, have shown the involvement of regulatory non-coding RNAs in the outbreak of
cancer cachexia. In particular, the role exerted by
microRNAs is being widely addressed, and several mechanistic studies are in progress. In this review, we discuss the most recent findings concerning the role of
microRNAs in triggering or exacerbating muscle wasting in
cancer cachexia, while mentioning about possible roles played by long non-coding RNAs and ADAR-mediated
miRNA modifications.