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ERα inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer

Xiao-Long Wei1,2, Xiao-Wei Dou2, Jing-Wen Bai2

  • 1Department of Pathology, Cancer Hospital of Shantou University Medical College, Shantou 515031, China.

Oncotarget
|May 30, 2015
PubMed

Insights

Estrogen receptor-alpha (ERα) inhibits breast cancer metastasis by downregulating Bmi1, a protein linked to tumor progression and stemness. This discovery offers new insights into ERα

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Estrogen receptor-alpha (ERα) is known to suppress epithelial-mesenchymal transition (EMT) and stemness in breast cancer, processes critical for metastasis.
  • The precise molecular mechanisms by which ERα exerts these regulatory effects are not fully understood.
  • Bmi1, a polycomb group protein, is implicated in EMT, stem cell self-renewal, and is overexpressed in various cancers.

Purpose of the Study:

  • To elucidate the mechanism by which ERα suppresses EMT and stemness in breast cancer.
  • To investigate the role of Bmi1 in ERα-mediated regulation of these processes.
  • To determine the clinical relevance of ERα and Bmi1 expression in human breast cancer tissues.

Main Methods:

  • Investigated the effect of ERα on E-cadherin expression and Bmi1 transcription in breast cancer cells.
  • Assessed the impact of ERα overexpression on cell migration, invasion, and EMT.
  • Evaluated the influence of ERα on cancer stem cell markers (CD44high/CD24low) and mammosphere formation capacity.
  • Examined the effect of Bmi1 overexpression on ERα-mediated suppression of EMT and stemness.
  • Performed immunohistochemistry to analyze ERα and Bmi1 expression in human breast cancer tissues.

Main Results:

  • ERα upregulated E-cadherin expression by transcriptionally downregulating Bmi1.
  • ERα overexpression suppressed breast cancer cell migration, invasion, and EMT.
  • ERα overexpression reduced the CD44high/CD24low cell population and inhibited mammosphere formation in ERα-negative cells.
  • Bmi1 overexpression counteracted the suppressive effects of ERα on EMT and stemness.
  • Immunohistochemistry revealed an inverse correlation between ERα and Bmi1 expression in human breast cancer tissues.

Conclusions:

  • ERα inhibits breast cancer cell EMT and stemness primarily through the downregulation of Bmi1.
  • ERα acts as a suppressor of key metastatic and stemness pathways by modulating Bmi1 expression.
  • The inverse relationship between ERα and Bmi1 in patient tissues supports their antagonistic roles in breast cancer progression.
Keywords:
Bmi1ERα signalingbreast cancerepithelial-mesenchymal transitionstemness

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