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NRF2 addiction in cancer cells
Hiroshi Kitamura1, Hozumi Motohashi1
1Department of Gene Expression Regulation, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
Cancer Science
|February 17, 2018
Summary
Persistent activation of the Kelch-like ECH-associated protein 1/nuclear factor erythroid-derived 2-like 2 (KEAP1-NRF2) system drives cancer growth and therapeutic resistance. New therapeutic targets beyond NRF2 are crucial for treating NRF2-addicted cancers effectively.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- The KEAP1-NRF2 system is vital for cellular defense against oxidative stress.
- Transient NRF2 activation benefits health, but persistent activation in cancer promotes malignancy and therapeutic resistance.
- Cancer cells can become addicted to high NRF2 activity, leading to aggressive phenotypes and poor prognoses.
Purpose of the Study:
- To review recent developments in understanding NRF2-addicted cancers.
- To explore potential therapeutic targets for these cancers.
- To discuss advances in diagnostics and therapeutics for NRF2-addicted cancers.
Main Methods:
- Literature review of studies on NRF2-addicted cancers.
- Analysis of NRF2's role in cancer cell proliferation and therapeutic resistance.
- Exploration of novel therapeutic strategies targeting NRF2 addiction.
Main Results:
- Persistent NRF2 activation confers increased antioxidant capacity, metabolic reprogramming, and therapeutic resistance to cancer cells.
- NRF2 addiction is linked to aggressive tumor behavior and poor patient outcomes.
- NRF2 inhibitors are under development, but systemic inhibition may cause adverse effects.
Conclusions:
- Targeting NRF2 addiction is a promising strategy for cancer therapy.
- Identifying alternative therapeutic targets is essential to mitigate side effects of systemic NRF2 inhibition.
- Advances in diagnostics and therapeutics are expected for NRF2-addicted cancers.
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