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The Keap1-Nrf2 system in cancers: stress response and anabolic metabolism

Yoichiro Mitsuishi1, Hozumi Motohashi, Masayuki Yamamoto

  • 1Department of Medical Biochemistry, Tohoku University Graduate School of Medicine Sendai, Japan ; Department of Respiratory Medicine, Tohoku University Graduate School of Medicine Sendai, Japan.

Frontiers in Oncology
|December 29, 2012
PubMed

Insights

The Keap1-Nrf2 pathway protects cells from stress. In cancer, Nrf2 stabilization promotes growth and resistance, suggesting Nrf2 inhibitors could be a therapeutic strategy.

Area of Science:

  • Cellular biology
  • Molecular mechanisms
  • Cancer research

Background:

  • The Keap1-Nrf2 pathway is crucial for cellular defense against oxidative and xenobiotic stresses.
  • Nrf2, a transcription factor, activates protective genes by binding to the antioxidant response element (ARE).
  • Under normal conditions, Keap1 targets Nrf2 for degradation; however, stress stabilizes Nrf2, leading to nuclear translocation and gene activation.

Purpose of the Study:

  • To review the Keap1-Nrf2 system's role in physiological and pathological conditions, particularly in cancer.
  • To present findings on Nrf2's function in cancer cell metabolism.
  • To discuss the therapeutic potential of targeting Nrf2 in cancer treatment.

Main Methods:

  • Literature review of the Keap1-Nrf2 pathway.
  • Analysis of Nrf2's role in cancer cell metabolism.
  • Discussion of Nrf2's impact on chemo- and radio-resistance.

Main Results:

  • Constitutive Nrf2 stabilization is observed in many human cancers, correlating with poor prognosis.
  • Nrf2 enhances cancer cell chemo- and radio-resistance through its antioxidant and detoxification functions.
  • Nrf2 likely promotes cancer cell growth by boosting cytoprotection and anabolism.

Conclusions:

  • The Keap1-Nrf2 pathway is a key player in cancer progression and treatment resistance.
  • Targeting Nrf2 may offer a promising strategy for cancer therapy.
  • Further research into Nrf2's metabolic functions could reveal new therapeutic avenues.
Keywords:
glutathionepurine nucleotideredox homeostasisstress responsetranscription

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