Mitochondrial ROS in cancer: Initiators, amplifiers or an Achilles' heel?

Simran S. Sabharwal, Paul T. Schumacker*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

648 Scopus citations

Abstract

Mitochondria cooperate with their host cells by contributing to bioenergetics, metabolism, biosynthesis, and cell death or survival functions. Reactive oxygen species (ROS) generated by mitochondria participate in stress signalling in normal cells but also contribute to the initiation of nuclear or mitochondrial DNA mutations that promote neoplastic transformation. In cancer cells, mitochondrial ROS amplify the tumorigenic phenotype and accelerate the accumulation of additional mutations that lead to metastatic behaviour. As mitochondria carry out important functions in normal cells, disabling their function is not a feasible therapy for cancer. However, ROS signalling contributes to proliferation and survival in many cancers, so the targeted disruption of mitochondria-to-cell redox communication represents a promising avenue for future therapy.

Original languageEnglish (US)
Pages (from-to)709-721
Number of pages13
JournalNature Reviews Cancer
Volume14
Issue number11
DOIs
StatePublished - Oct 27 2014

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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