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Year : 2021  |  Volume : 8  |  Issue : 4  |  Page : 452-458

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

1 Department of Public Health and Infectious Diseases, Sapienza University of Rome, Rome, Italy
2 School of Population and Public Health, University of British Columbia, Vancouver, BC, Canada
3 Frimley Park Hospital, Camberley, United Kingdom
4 Wythenshawe Hospital, Manchester University NHS Foundation Trust, Manchester, United Kingdom
5 National Institute of Urology and Nephrology, Cairo, Egypt
6 Aberdeen Royal Infirmary, Aberdeen, United Kingdom

Correspondence Address:
Dr. Chidiebere Emmanuel Okechukwu
Department of Public Health and Infectious Diseases, Sapienza University of Rome, Piazzale Aldo Moro 5 – 00185 Rome.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mgmj.mgmj_67_21

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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.

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