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Updated: Sep 20, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

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Long non-coding RNA NORAD suppresses erastin-induced ferroptosis in breast cancer by upregulating SLC7A11 via

Pengfei Shi1, Bo Hu1, Yongjun Liu1

  • 1Department of Thyroid and Breast Surgery, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

International Journal of Surgery (London, England)
|May 23, 2025
PubMed
Abstract

Insights

Non-coding RNA activated by DNA damage (NORAD) suppresses ferroptosis in breast cancer (BC) by upregulating SLC7A11. This finding reveals NORAD as a potential therapeutic target for BC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Death Research

Background:

  • Ferroptosis, a form of iron-dependent cell death, is a known impediment to various cancers, including breast cancer (BC).
  • High expression of non-coding RNA activated by DNA damage (NORAD) correlates with poor prognosis in BC patients.
  • The specific role of NORAD in BC ferroptosis remains largely unexplored.

Purpose of the Study:

  • To investigate the role of NORAD in regulating ferroptosis in breast cancer cells.
  • To elucidate the molecular mechanism by which NORAD influences ferroptosis.
  • To assess the in vivo effect of NORAD on breast cancer ferroptosis.

Main Methods:

  • Breast cancer cells were treated with erastin to induce ferroptosis.
  • Western blotting and qPCR assessed molecular levels; CCK-8 assays evaluated cell viability.
  • Mechanisms were explored using ChIP, luciferase reporter, and RIP assays; in vivo studies utilized a xenograft mouse model.

Main Results:

  • NORAD was highly expressed in human BC tissues and cells.
  • NORAD overexpression inhibited erastin-induced ferroptosis, while silencing facilitated it.
  • NORAD upregulated NR3C1 via FUS interaction, which in turn upregulated SLC7A11, reversing ferroptosis promotion by NORAD silencing.

Conclusions:

  • NORAD suppresses erastin-induced ferroptosis in breast cancer cells.
  • This suppression occurs through the FUS/NR3C1 axis, leading to the upregulation of SLC7A11.
  • NORAD's role in ferroptosis suppression suggests it as a potential therapeutic target for breast cancer.
Keywords:
NORADSLC7A11breast cancererastinferroptosis

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