Escaping death: Mitochondrial redox homeostasis in cancer cells

Francesco Ciccarese, Vincenzo Ciminale

Research output: Contribution to journalReview articlepeer-review


Reactive oxygen species (ROS) are important signaling molecules that act through the oxidation of nucleic acids, proteins, and lipids. Several hallmarks of cancer, including uncontrolled proliferation, angiogenesis, and genomic instability, are promoted by the increased ROS levels commonly found in tumor cells. To counteract excessive ROS accumulation, oxidative stress, and death, cancer cells tightly regulate ROS levels by enhancing scavenging enzymes, which are dependent on the reducing cofactor nicotinamide adenine dinucleotide phosphate (NADPH). This review focuses on mitochondrial ROS homeostasis with a description of six pathways of NADPH production in mitochondria and a discussion of the possible strategies of pharmacological intervention to selectively eliminate cancer cells by increasing their ROS levels.

Original languageEnglish
Article number117
JournalFrontiers in Oncology
Issue numberJUN
Publication statusPublished - Jun 9 2017


  • Apoptosis
  • Cancer metabolism
  • Mitochondria
  • Nicotinamide adenine dinucleotide phosphate
  • Reactive oxygen species

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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