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Updated: Mar 19, 2026

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NRF2, a Key Regulator of Antioxidants with Two Faces towards Cancer

Jaieun Kim1, Young-Sam Keum2

  • 1Department of Pathology, College of Korean Medicine, Dongguk University, Donggukro 32, Goyang, Gyeonggi-do 10326, Republic of Korea.

Oxidative Medicine and Cellular Longevity
|June 25, 2016
PubMed

Insights

Reactive oxygen species (ROS) are vital for cell signaling but can be harmful. The transcription factor NRF2 (NF-E2-related factor-2) protects against stress, though cancer cells exploit NRF2 for survival.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Reactive oxygen species (ROS) play dual roles in cellular functions, acting as signaling molecules at low levels and causing damage at high levels.
  • Organisms possess antioxidant systems and the transcription factor NRF2 (NF-E2-related factor-2) to manage oxidative stress.
  • While NRF2 activation is generally protective, cancer cells increasingly utilize NRF2 to survive under oxidative stress conditions.

Purpose of the Study:

  • To review the molecular mechanisms, structure, and function of the KEAP1-NRF2 interaction.
  • To discuss the dual role of NRF2 activity in cancer, highlighting its protective and detrimental aspects.

Main Methods:

  • Literature review focusing on the KEAP1-NRF2 pathway.
  • Analysis of recent studies on NRF2 activity in cancer.

Main Results:

  • Detailed overview of the KEAP1-NRF2 interaction, a critical regulator of cellular response to oxidative stress.
  • Evidence showing cancer cells co-opting NRF2 to enhance survival under oxidative stress.

Conclusions:

  • Understanding the KEAP1-NRF2 interaction is crucial for deciphering cellular stress responses.
  • The role of NRF2 in cancer is complex, presenting both challenges and therapeutic opportunities, necessitating careful consideration of its activity.

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