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Related Experiment Video

Updated: May 12, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

E47 and Id1 interplay in epithelial-mesenchymal transition.

Eva Cubillo¹, Antonio Diaz-Lopez, Eva P Cuevas

¹Departamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM), Instituto de Investigaciones Biomédicas Alberto Sols (CSIC-UAM), IdiPAZ, Madrid, Spain.

|April 5, 2013

Summary

E47 and Id1 proteins collaborate to maintain epithelial-mesenchymal transition (EMT) in cancer cells. This interaction is crucial for the mesenchymal phenotype, independent of Id1

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Published on: October 27, 2020

Area of Science:

Molecular Biology
Cell Biology
Cancer Research

Background:

Epithelial-mesenchymal transition (EMT) is a process implicated in cancer progression.
E47 (a transcription factor) and Id1 (an inhibitor) are involved in EMT.
Previous work showed E47 induces EMT with Id1/Id3 overexpression.

Purpose of the Study:

To investigate the interaction between E47 and Id1 in EMT.
To determine the role of this interaction in maintaining the mesenchymal phenotype.
To explore the clinical relevance of E47 and Id1 in breast cancer.

Main Methods:

Cell culture (MDCK, breast carcinoma, melanoma cells)
Co-immunoprecipitation assays to detect protein interactions.
Chromatin immunoprecipitation (ChIP) assays to assess promoter binding.
Analysis of breast tumor series (N0) for gene expression.

Main Results:

E47 interacts with Id1 in mesenchymal cells.
E47 binds directly to the E-cadherin promoter without Id1.
Both E47 and Id1 are essential for maintaining the mesenchymal phenotype.
E47 and Id1 expression correlates with basal-like breast cancer phenotype.

Conclusions:

E47 and Id1 cooperate to maintain EMT through mechanisms independent of Id1's dominant-negative effect on E47 binding.
The E47-Id1 association is biologically significant in basal-like breast cancer.