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Mechanism and regulation of epithelial–mesenchymal transition in cancer

Authors Guttilla Reed I

Received 27 June 2015

Accepted for publication 22 July 2015

Published 20 August 2015 Volume 2015:7 Pages 155—166


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Professor Denis Wirtz

Irene K Guttilla Reed

Department of Biology, University of Saint Joseph, West Hartford, CT, USA

Abstract: During development and the pathogenesis of certain diseases, including cancer, the epithelial–mesenchymal transition (EMT) program is activated. It is hypothesized that EMT plays a major role in tumor invasion and the establishment of distant metastases. Metastatic disease is responsible for the vast majority of cancer-related deaths, which provides a precedent for elucidating pathways that regulate EMT. EMT is defined as the transition of cells with an epithelial phenotype into cells with a mesenchymal phenotype through a series of genetic and environmental events. This leads to the repression of epithelial-associated markers, upregulation of mesenchymal-associated markers, a loss of cell polarity and adhesion, and increased cell motility and invasiveness. EMT is a reversible and dynamic process, and can be regulated by signals from the microenvironment such as inflammation, hypoxia, and growth factors or epigenetically via microRNAs. These signals modulate key EMT-associated transcription factors and effector proteins that control cellular phenotype and regulate tumor plasticity in response to changing conditions in the microenvironment and the progressive nature of cancer. Understanding the complex regulatory networks controlling EMT can provide insight into tumor progression and metastasis.

Keywords: EMT, metastasis, microRNA, transcription factor, growth factor, tumor progression

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