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NR4A1 suppresses breast cancer growth by repressing c-Fos-mediated lipid and redox dyshomeostasis

Cen Jiang1, Youzhi Zhu2,3, Junsi Zhang2

  • 1Central Laboratory, Fujian Medical University Union Hospital, Fuzhou, China. ajiangcen@126.com.

Experimental & Molecular Medicine
|March 31, 2025
PubMed

Insights

Nuclear receptor subfamily 4 group A member 1 (NR4A1) suppresses breast cancer (BC) growth by regulating lipid metabolism and oxidative stress. Activating NR4A1 may offer a new therapeutic strategy for BC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The role of NR4A1 (Nuclear Receptor subfamily 4 group A member 1) in cancer, particularly breast cancer (BC), is not fully understood.
  • NR4A1's function as a transcriptional regulator in cancer warrants further investigation.

Purpose of the Study:

  • To elucidate the biological function of NR4A1 in suppressing breast cancer growth.
  • To investigate the molecular mechanisms underlying NR4A1's effects on BC progression.
  • To explore NR4A1 as a potential therapeutic target for breast cancer.

Main Methods:

  • Correlation analysis of NR4A1 deficiency with BC progression in clinical data.
  • Genetic deletion and knockout of NR4A1 in BC cell lines.
  • Global metabolome screening to analyze metabolic changes.
  • Transcriptomic and epigenomic analyses to identify molecular targets.
  • Treatment with NR4A1 agonist cytosporone B and assessment of its effects.

Main Results:

  • NR4A1 deficiency correlates with BC progression and promotes proliferation and tumor growth.
  • NR4A1 deletion leads to lipid remodeling, phospholipid accumulation, and increased fatty acid/lipid uptake.
  • NR4A1 knockout induces oxidative stress and disrupts redox balance.
  • NR4A1 restrains BC proliferation by inhibiting c-Fos binding to the PRDX6 promoter, affecting lipid and redox homeostasis.
  • NR4A1 agonist cytosporone B activates NR4A1, enhances NR4A1-c-Fos interaction, and inhibits BC cell growth.

Conclusions:

  • NR4A1 plays a crucial role in suppressing breast cancer growth by regulating lipid metabolism and oxidative stress.
  • NR4A1 acts by interacting with c-Fos to control the expression of genes involved in homeostasis.
  • NR4A1 agonists represent a promising therapeutic strategy for breast cancer treatment.

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