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Related Experiment Video

Updated: Sep 13, 2025

Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
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Long-Chain Fatty Acids Alter Estrogen Receptor Expression in Breast Cancer Cells.

Ruiko Ogata1, Yi Luo1, Rina Fujiwara-Tani1

  • 1Department of Molecular Pathology, Nara Medical University School of Medicine, Kashihara 634-8521, Japan.

International Journal of Molecular Sciences
|July 29, 2025
PubMed
Summary

Long-chain fatty acids impact breast cancer by altering estrogen receptor (ER) expression. Specific fatty acids like oleic acid decrease ER in some cells, while palmitic acid increases it in others, affecting treatment response.

Keywords:
breast cancerestrogen receptorlong-chain fatty acidtriple negative breast cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Nutritional Science

Background:

  • Long-chain fatty acids (LCFAs) are recognized regulators of cancer metabolism.
  • The influence of LCFAs on hormone receptor expression in breast cancer (BCA) is not well understood.

Purpose of the Study:

  • To investigate the effects of five LCFAs on hormone receptor expression in two distinct breast cancer cell lines.
  • To elucidate the mechanisms by which LCFAs modulate estrogen receptor alpha (ERα) expression and signaling.

Main Methods:

  • Treatment of MCF7 (luminal) and MDA-MB-231 (triple-negative) breast cancer cells with five LCFAs: linoleic acid, oleic acid, elaidic acid, palmitic acid, and α-linolenic acid.
  • Assessment of cell viability, mitochondrial function, reactive oxygen species production, and metabolic shifts.
  • Analysis of estrogen receptor alpha (ERα) mRNA and protein levels.
  • MicroRNA profiling to identify regulatory microRNAs.

Main Results:

  • All tested LCFAs reduced cell viability and mitochondrial function in a dose-dependent manner.
  • Oleic acid (OA) decreased ERα mRNA and protein in MCF7 cells, reducing responsiveness to estradiol and tamoxifen.
  • Palmitic acid (PA) increased ERα protein in MB231 cells, though ER signaling remained inactive.
  • OA upregulated miR-22 and miR-221 in MCF7, while PA increased miR-34a in MB231, correlating with ERα modulation.

Conclusions:

  • Specific LCFAs differentially regulate ERα expression and signaling in breast cancer cells through epigenetic and post-transcriptional mechanisms.
  • Dietary lipids can influence breast cancer therapeutic efficacy by modulating nuclear receptor signaling pathways.
  • These findings provide novel insights into the interplay between dietary lipids, hormone receptor status, and breast cancer progression.