MnSOD/SOD2 in Cancer: The Story of a Double Agent

  • Juan C. Mayo Morphology and Cell Biology department, University of Oviedo. Oviedo, Asturias, Spain
  • Rosa M. Sainz Morphology and Cell Biology department, University of Oviedo. Oviedo, Asturias, Spain
  • Isabel Quiros-Gonzalez CRUK Cambridge Institute, University of Cambridge, Cambridge, UK
Keywords: Differentiation; Gene regulation; MnSOD; Senescence; Tumor suppressor; Tumorigenesis

Abstract

Manganese-dependent superoxide dismutase (MnSOD/SOD2) is one of the major antioxidant enzymes which scavenges the superoxide produced in the mitochondria, the main source of free radicals in non-pathological conditions. This first barrier is important to prevent early stages of cancer development. However, once the tumor is established, upregulation of MnSOD without a concomitant increase of scavengers of hydrogen peroxide (H2O2) plays a much complex role. It contributes to proliferation, angiogenesis and invasion, affecting glycolytic metabolism and preventing the mitochondria from inducing apoptosis favoring therapy resistance. The increase of H2O2 mediated by MnSODis able to induce phenotypical changes in several tumor types, such as epithelia-mesenchymal transition increasing the motility of tumor cells, neuroendocrine differentiation and senescent secretory phenotypes which feed tumor progression by producing cytokines and growth factors.

Published
2018-03-01
How to Cite
Mayo, J., Sainz, R., & Quiros-Gonzalez, I. (2018). MnSOD/SOD2 in Cancer: The Story of a Double Agent. Reactive Oxygen Species, 5(14), 86–106. Retrieved from https://www.aimsci.com/ros/index.php/ros/article/view/128
Section
Review Articles