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Oxidative Stress and Cancer: The Role of Nrf2

Soraya Sajadimajd1, Mozafar Khazaei1

  • 1Fertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Current Cancer Drug Targets
|October 4, 2017
PubMed

Insights

Oxidative stress impacts cell fate, with excessive reactive oxygen species (ROS) promoting cancer. The NRF2 pathway regulates cellular defense, but its deregulation can lead to cancer progression and treatment resistance.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Oxidative stress, an imbalance in reactive oxygen species (ROS) production and detoxification, critically influences cell fate.
  • Excessive ROS can trigger apoptosis for normal cell death, but also promote carcinogenesis by deregulating biomolecules in cells with faulty signaling.
  • The Nuclear factor erythroid 2-related factor 2 (NRF2) is a master regulator protecting cells against oxidative and electrophilic stress.

Purpose of the Study:

  • To elucidate the role of the NRF2 signaling pathway in cellular response to oxidative stress and its implications in carcinogenesis.
  • To understand the regulatory mechanisms of NRF2 activation and its link to cancer development, including proliferation, metastasis, and chemoresistance.
  • To explore the potential of NRF2 modulation in personalized cancer therapy.

Main Methods:

  • Review of existing literature on oxidative stress, ROS, NRF2, Keap1, and their roles in cellular processes and cancer.
  • Analysis of the molecular mechanisms governing NRF2 activation, including its interaction with Keap1 and the impact of ROS.
  • Examination of the consequences of NRF2/Keap1 deregulation in cancer, such as mutations and oncogene activation.

Main Results:

  • NRF2 controls the expression of genes encoding antioxidant enzymes, detoxifying factors, anti-apoptotic proteins, and drug transporters.
  • Under oxidative stress, ROS triggers the dissociation of the NRF2:Keap1 complex, leading to NRF2 nuclear import and activation of cytoprotective genes.
  • Deregulation of NRF2/Keap1 is linked to constitutive NRF2 activation, promoting cancer cell survival, proliferation, metastasis, and chemoresistance.

Conclusions:

  • The interplay between ROS and NRF2 signaling is crucial in the development and progression of cancer.
  • Aberrant NRF2 activation confers survival advantages to cancer cells, contributing to therapeutic challenges.
  • Targeting the NRF2 pathway holds promise for developing novel, personalized cancer treatment strategies.
Keywords:
AntioxidantCancerKeap1Nrf2Oxidative stressROS.

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