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Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
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ESR1-Activating Mutations Confer Metabolic Vulnerabilities in ER+ Breast Cancer.

Francesca Bonechi1, Marina Bacci1, Nicla Lorito1

  • 1Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy.

Cancer Research
|November 7, 2025
PubMed
Summary

Estrogen receptor-1 (ESR1) mutations in breast cancer create vulnerabilities in lipid metabolism, making tumors sensitive to ferroptosis. Combining ferroptosis inducers with endocrine therapy shows promise for treating resistant ER+ breast cancer.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Pathways

Background:

  • Endocrine therapy (ET) is standard for estrogen receptor-positive (ER+) breast cancer.
  • Estrogen receptor-1 (ESR1) mutations are rare initially but common in ET-resistant breast cancer.

Purpose of the Study:

  • Investigate the impact of ESR1 mutations on breast cancer lipid metabolism.
  • Identify new therapeutic strategies for ET-resistant ER+ breast cancer.

Main Methods:

  • Analysis of ESR1 mutations in preclinical models and patient-derived ER+ breast cancer.
  • Assessment of lipid metabolism, acyl-CoA synthetase long-chain family member 4 (ACSL4) expression, and ferroptosis sensitivity.
  • Evaluation of combination therapy with ferroptosis inducers and selective estrogen receptor degraders (SERDs).

Main Results:

  • ESR1 mutations induce constitutive estrogen receptor (ER) activation, driving aberrant lipid biogenesis and increasing ACSL4 expression.
  • ESR1 mutations sensitize ER+ breast cancer cells to ferroptosis, overcoming inherent resistance.
  • Ferroptosis inducers enhance the efficacy of fulvestrant and elacestrant in preclinical models and patient-derived material.

Conclusions:

  • ESR1 mutations create vulnerabilities in lipid metabolism, making ER+ breast cancer susceptible to ferroptosis.
  • Combination therapy with ferroptosis inducers and SERDs is a promising strategy for ET-resistant breast cancer.
  • ACSL4 serves as a potential biomarker for identifying ER+ breast cancers sensitive to ferroptosis induction.