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Related Experiment Video

Updated: Jan 9, 2026

Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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RAD51B-EZH2 axis as a potential therapeutic target for TNBC through cell fate conversion.

Shiqi Lin1,2,3, Dongyang Tang1,2, Josh Haipeng Lei1,2

  • 1MOE Frontier Science Center for Precision Oncology, University of Macau, Macau SAR, China.

Cell Death & Disease
|November 29, 2025
PubMed
Summary

Triple-negative breast cancer (TNBC) is aggressive, lacking targets. Rad51b deficiency represses ERα, creating TNBC. Targeting the RAD51B-EZH2 axis re-expresses ERα, making TNBC treatable with endocrine therapy.

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Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited therapeutic targets.
  • Identifying novel molecular drivers is crucial for developing effective treatments for TNBC.

Purpose of the Study:

  • To identify candidate driver genes involved in TNBC formation.
  • To elucidate the molecular mechanisms underlying TNBC development and identify potential therapeutic targets.

Main Methods:

  • Utilized the Sleeping Beauty (SB) transposon system for functional screening in mouse models (Brca1-deficient and Fgfr2-mutant).
  • Investigated the role of Rad51b deficiency in TNBC development and ERα repression.
  • Analyzed the involvement of Polycomb Repressive Complex 2 (PRC2), histone modifications, and the AMPK pathway.

Main Results:

  • Identified 64 overlapped candidate driver genes for TNBC induction.
  • Demonstrated that Rad51b deficiency represses estrogen receptor alpha (ERα) expression via PRC2 recruitment and H3K27 trimethylation.
  • Showed that RAD51B loss upregulates ATP, suppresses AMPK, and dephosphorylates EZH2, enhancing PRC2 activity and repressing Esr1.

Conclusions:

  • The RAD51B-EZH2 axis is a key regulator of ERα expression in TNBC.
  • Inhibiting this axis can restore ERα expression, rendering TNBC susceptible to endocrine therapy.
  • Combination therapy with an EZH2 inhibitor and tamoxifen shows promise in reducing TNBC progression.