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Updated: Sep 27, 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 Slug represses E-cadherin expression and induces epithelial to mesenchymal transitions: a

Victoria Bolós1, Hector Peinado, Mirna A Pérez-Moreno

  • 1Instituto de Investigaciones Biomédicas "Alberto Sols" (CSIC-UAM), Arturo Duperier, 4, 28029 Madrid, Spain.

Journal of Cell Science
|January 1, 2003
PubMed

Insights

The Snail family member Slug represses E-cadherin transcription, driving epithelial to mesenchymal transition. Its binding affinity to E-cadherin promoter elements is lower than other repressors, suggesting context-dependent regulation.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Cancer Research

Background:

  • E-cadherin downregulation is critical for development and tumor progression.
  • Several transcriptional repressors (Snail, E12/E47, ZEB-1, SIP-1) target E-cadherin via promoter E-boxes.

Purpose of the Study:

  • To investigate the role of the Snail family member Slug in E-cadherin repression.
  • To determine the mechanism of Slug-mediated E-cadherin downregulation.

Main Methods:

  • Stable expression of Slug in MDCK cells.
  • Analysis of E-cadherin transcriptional levels.
  • Investigation of Slug binding to E-cadherin promoter elements (E-pal).
  • Comparative binding affinity studies of Slug versus other repressors.

Main Results:

  • Slug acts as a repressor of E-cadherin transcription.
  • Stable Slug expression induces a complete epithelial to mesenchymal transition.
  • Slug binds to E-cadherin promoter E-boxes, specifically the E-pal element.
  • Slug exhibits lower binding affinity to the E-pal element compared to Snail and E47.

Conclusions:

  • Slug contributes to E-cadherin repression and epithelial to mesenchymal transition.
  • Slug-mediated repression involves binding to E-cadherin promoter E-boxes.
  • The in vivo activity of E-cadherin repressors is modulated by relative concentrations and cellular context.

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