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Genetic, metabolic and immunological features of cancers with NRF2 addiction

Hiroshi Kitamura1, Haruna Takeda1, Hozumi Motohashi1

  • 1Department of Gene Expression Regulation, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.

FEBS Letters
|July 28, 2022
PubMed

Insights

Nuclear factor erythroid-derived 2-like 2 (NRF2) is crucial for cellular defense but detrimental when activated in cancer. This review explores the genetic, metabolic, and immune features of NRF2-addicted cancer cells and their therapeutic potential.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cellular Defense Mechanisms

Background:

  • Nuclear factor erythroid-derived 2-like 2 (NRF2) is a key transcription factor regulating cytoprotective genes against oxidative stress.
  • While beneficial in normal cells, sustained NRF2 activation in cancer cells drives malignant progression and therapeutic resistance, leading to 'NRF2 addiction'.

Purpose of the Study:

  • To summarize recent findings on the characteristics of NRF2-activated cancer cells.
  • To discuss the prerequisites for NRF2 addiction in cancer.
  • To explore therapeutic strategies targeting NRF2-addicted cancers.

Main Methods:

  • Review of recent scientific literature and data.
  • Analysis of genetic, metabolic, and immunological features of cancer cells.
  • Discussion of therapeutic applications based on NRF2 dependency.

Main Results:

  • NRF2 activation provides significant advantages to cancer cells, promoting tumor growth and resistance.
  • Normal cells cannot tolerate the persistent NRF2 activation seen in malignant cells.
  • Specific cellular requirements enable cancer cells to exploit NRF2 for malignant evolution.

Conclusions:

  • Understanding the features of NRF2-addicted cancer cells is crucial for developing targeted therapies.
  • Identifying the prerequisites for NRF2 addiction may reveal new therapeutic vulnerabilities.
  • Targeting NRF2 addiction holds promise for treating various human cancers.
Keywords:
CEBPBKEAP1NOTCH3NRF2cancer stemnessimmunoevasionmalignancymetabolic reprogrammingnon-small cell lung cancerpentose phosphate pathway

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