Redox regulation of tumor suppressor PTEN in cancer and aging (Review)

Int J Mol Med. 2013 Mar;31(3):511-5. doi: 10.3892/ijmm.2013.1235. Epub 2013 Jan 10.


Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) has been shown to act as a tumor suppressor whose function includes important roles in regulating oxidative stress, indicating a potential role in oxidative damage-associated cancer. Accumulating evidence has revealed that PTEN also acts as a pivotal determinant of cell fate, regarding senescence and apoptosis, which is mediated by intracellular reactive oxygen species (ROS) generation. Cells are continuously exposed to ROS, which represent mutagens and are thought to be a major contributor to cancer and the aging process. Therefore, cellular ROS sensing and metabolism are firmly regulated by a variety of proteins involved in the redox mechanism. In this review, PTEN and the roles of oxidative stress in phosphoinositide-3 kinase/AKT signaling are summarized with a focus on the links between the pathways and ROS in cancer and aging.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Apoptosis
  • Cellular Senescence*
  • Humans
  • Mitochondria / metabolism
  • Neoplasms / metabolism*
  • Oxidation-Reduction
  • Oxidative Stress
  • PTEN Phosphohydrolase / biosynthesis
  • PTEN Phosphohydrolase / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction


  • Reactive Oxygen Species
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human