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Genetic and epigenetic regulation of the NRF2-KEAP1 pathway in human lung cancer

Nuria Camiña1, Trevor M Penning2

  • 1Department of Systems Pharmacology & Translational Therapeutics, Center of Excellence in Environmental Toxicology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

British Journal of Cancer
|November 30, 2021
PubMed

Insights

The nuclear factor erythroid 2-related factor 2 (NRF2) pathway protects against cellular stress but can promote cancer. Its epigenetic regulation in lung cancer is crucial for understanding oncogenesis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • Cellular stress from electrophiles and oxidation disrupts homeostasis.
  • The nuclear factor erythroid 2-related factor 2 (NRF2) pathway is a key defense mechanism.
  • NRF2 activation can detoxify carcinogens but also promote cancer in specific contexts.

Purpose of the Study:

  • To review the activation of the NRF2-KEAP1 signaling pathway in human lung cancer.
  • To explore the epigenetic regulation of NRF2 and KEAP1.
  • To understand the role of this pathway in oncogenesis.

Main Methods:

  • Review of existing literature on NRF2-KEAP1 pathway.
  • Analysis of epigenetic mechanisms (DNA methylation, histone modification, microRNA) regulating NFE2L2 and KEAP1.
  • Examination of NRF2 target genes as biomarkers of stress signaling.

Main Results:

  • NRF2 activation is a double-edged sword in cancer, offering protection and promotion.
  • Epigenetic modifications significantly influence NFE2L2 expression and NRF2 pathway activity.
  • NRF2 target genes serve as indicators of cellular stress responses.

Conclusions:

  • Understanding NRF2-KEAP1 pathway epigenetics in lung cancer is vital for therapeutic strategies.
  • Epigenetic dysregulation of NRF2 contributes to lung cancer development.
  • Targeting the NRF2 pathway, considering its epigenetic modulation, holds potential for cancer treatment.

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