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Updated: Jul 12, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

The transcription factor snail mediates epithelial to mesenchymal transitions by repression of estrogen

Archana Dhasarathy1, Masahiro Kajita, Paul A Wade

  • 1Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, P.O. Box 12233, 111 TW Alexander Drive, Research Triangle Park, North Carolina 27709, USA.

Molecular Endocrinology (Baltimore, Md.)
|September 1, 2007
PubMed

Insights

Estrogen receptor-alpha (ESR1) loss in breast cancer promotes metastasis. Snail expression decreases cell adhesion and ER-alpha levels, activating TGF-beta signaling, which drives cancer cell invasion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Estrogen receptor (ER)-alpha (ESR1) is crucial for mammary cell development and its loss correlates with poor breast cancer prognosis.
  • ER-alpha may constrain invasive growth by regulating metastasis-associated protein 3 (MTA3), which represses Snail, a factor in epithelial to mesenchymal transition (EMT).

Purpose of the Study:

  • To investigate the role of Snail in epithelial to mesenchymal transition (EMT) within the context of ER-alpha positive breast cancer cells.
  • To elucidate the molecular mechanisms linking ER-alpha, Snail, and TGF-beta signaling in breast cancer progression.

Main Methods:

  • Expressed Snail in the ER-alpha positive MCF-7 breast cancer cell line.
  • Assessed changes in cell-cell adhesion, cell invasiveness, and ER-alpha expression (RNA and protein levels).
  • Investigated Snail interaction with ESR1 regulatory DNA and analyzed TGF-beta pathway components.

Main Results:

  • Snail expression decreased cell-cell adhesion and increased invasiveness in MCF-7 cells.
  • Snail expression led to a significant reduction in both ER-alpha RNA and protein levels.
  • Snail directly interacted with regulatory regions of the ESR1 locus, and TGF-beta pathway components were upregulated.

Conclusions:

  • Snail-induced loss of ER-alpha function promotes breast cancer cell invasiveness.
  • Cross-talk between ER-alpha, Snail, and TGF-beta signaling pathways critically influences breast cancer cell phenotypes.
  • Understanding these interactions may reveal new therapeutic targets for metastatic breast cancer.

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