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Updated: Oct 30, 2025

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing
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Published on: June 9, 2017

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Nrf2 in Cancer, Detoxifying Enzymes and Cell Death Programs

Tabitha Jenkins1, Jerome Gouge1

  • 1Institute of Structural and Molecular Biology, Birkbeck College, University of London, London WC1E 7HX, UK.

Antioxidants (Basel, Switzerland)
|July 2, 2021
PubMed

Insights

Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates cellular defense against oxidative stress. While protective in healthy cells, its overactivation in cancer promotes tumor growth and resistance to cell death.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Reactive oxygen species (ROS) are vital for cell signaling but can damage cellular components.
  • Cells maintain redox balance via complex pathways, with Nrf2 (Nuclear factor erythroid 2-related factor 2) being a key regulator.
  • Nrf2 activation under oxidative stress induces detoxification and antiapoptotic factors.

Purpose of the Study:

  • To review the activation and function of the Nrf2 pathway.
  • To explore the role of Nrf2 dysregulation in cancer.
  • To discuss Nrf2's involvement in preventing apoptosis and ferroptosis in cancer.

Main Methods:

  • Literature review focusing on Nrf2 pathway activation, DNA binding, and cancer-related dysregulation.
  • Analysis of Nrf2's role in apoptosis and ferroptosis evasion.
  • Exploration of Nrf2's link to selenium-containing detoxifying enzymes.

Main Results:

  • Nrf2 is activated in the cytoplasm under oxidative stress.
  • Constitutive Nrf2 activation in cancer fuels tumor growth and metastasis.
  • Nrf2 plays a significant role in cancer cells evading programmed cell death, including apoptosis and ferroptosis.

Conclusions:

  • The Nrf2 pathway is a critical regulator of cellular redox homeostasis with dual roles in health and disease.
  • Dysregulation of Nrf2 in cancer contributes to tumorigenesis and resistance to therapy.
  • Further research into Nrf2's interaction with detoxifying enzymes may reveal new therapeutic strategies.
Keywords:
Brf2GPx4Nrf2SecTRAPsTrxR1canceroxidative stressselenoproteinstranscription

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