Hypothesized biological mechanisms by which exercise-induced irisin mitigates tumor proliferation and improves cancer treatment outcomes

Exercise has been linked to a significant decrease in cancer pathogenesis. Irisin is an exercise-induced myokine that is released from the skeletal muscle upon cleavage of the membrane of fibronectin type III domain-containing protein 5. Exercise has been revealed to raise irisin concentration in the blood and muscle cells via the upregulation of peroxisome proliferator receptor γ coactivator-1α expression. Exercise-induced irisin reduces the risk of numerous cancers by burning excess body fat. We hypothesized that exercise-induced irisin may mitigate tumor proliferation by inducing apoptosis and improving cancer treatment outcomes via modulating several signaling and metabolic pathways, mainly by increasing the phosphorylation of adenosine monophosphate-activated protein kinase and acetyl-CoA-carboxylase, via deactivating the phosphatidylinositol 3-kinase/protein kinase B Snail signaling pathway, by upregulating the apoptosis pathway through the inhibition of epithelial–mesenchymal transition and via stimulating caspase activity.