Mitochondrial reactive oxygen species and cancer

Lucas B. Sullivan, Navdeep Chandel*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

Abstract

Mitochondria produce reactive oxygen species (mROS) as a natural by-product of electron transport chain activity. While initial studies focused on the damaging effects of reactive oxygen species, a recent paradigm shift has shown that mROS can act as signaling molecules to activate pro-growth responses. Cancer cells have long been observed to have increased production of ROS relative to normal cells, although the implications of this increase were not always clear. This is especially interesting considering cancer cells often also induce expression of antioxidant proteins. Here, we discuss how cancer-associated mutations and microenvironments can increase production of mROS, which can lead to activation of tumorigenic signaling and metabolic reprogramming. This tumorigenic signaling also increases expression of antioxidant proteins to balance the high production of ROS to maintain redox homeostasis. We also discuss how cancer-specific modifications to ROS and antioxidants may be targeted for therapy.

Original languageEnglish (US)
Article number17
JournalCancer and Metabolism
Volume2
Issue number1
DOIs
StatePublished - Nov 28 2014

Keywords

  • Antioxidants
  • Cancer
  • Metabolism
  • Mitochondria reactive oxygen species
  • Oxidative stress
  • ROS

ASJC Scopus subject areas

  • Oncology
  • Cancer Research
  • Endocrinology, Diabetes and Metabolism

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