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Related Experiment Video

Updated: May 31, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Vimentin: Central hub in EMT induction?

Johanna Ivaska¹

¹Medical Biotechnology; VTT Technical Research Centre of Finland; Turku Centre for Biotechnology and Department of Biochemistry and Food Chemistry; University of Turku; Turku, Finland.

|June 21, 2011

Summary

This summary is machine-generated.

Vimentin, an intermediate filament protein, drives cell motility and metastasis during epithelial-to-mesenchymal transition (EMT). This study reveals vimentin actively promotes EMT by upregulating key genes, including Axl, essential for cancer cell migration.

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Last Updated: May 31, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition

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Published on: August 27, 2013

An Enzyme- and Serum-free Neural Stem Cell Culture Model for EMT Investigation Suited for Drug Discovery

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Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Published on: October 9, 2014

Area of Science:

Cell Biology
Molecular Biology
Cancer Research

Background:

Epithelial-to-mesenchymal transition (EMT) is crucial for cell motility, survival, development, and cancer metastasis.
Vimentin, an intermediate filament protein, is upregulated during EMT and traditionally viewed as a marker.
The functional role of vimentin in the EMT process has remained largely undefined.

Purpose of the Study:

To elucidate the functional contribution of vimentin in epithelial-to-mesenchymal transition (EMT).
To investigate the regulatory mechanisms by which vimentin influences EMT-associated gene expression and cell migration.

Main Methods:

Gene expression analysis to identify EMT-linked genes regulated by vimentin.
Investigation of vimentin's role in regulating receptor tyrosine kinase Axl expression.
Assessment of vimentin's impact on EMT-induced cell migration.

Main Results:

Vimentin actively contributes to EMT by upregulating the expression of several EMT-linked genes.
Vimentin specifically regulates EMT-associated migration through the upregulation of receptor tyrosine kinase Axl.
Upregulation of vimentin is demonstrated to be a prerequisite for EMT induction.

Conclusions:

Vimentin functions as a positive regulator of EMT, not merely a marker.
Vimentin's role in upregulating Axl expression is critical for EMT-induced cell migration.
Targeting vimentin may offer therapeutic strategies for inhibiting cancer metastasis.