IMR Press / FBS / Volume 4 / Issue 2 / DOI: 10.2741/S292

Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
EGF-receptor signaling and epithelial-mesenchymal transition in human carcinomas
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1 Syrian Research Cancer Centre of the Syrian Society against Cancer, Aleppo, Syria
2 Oncology Department, Faculty of Medicine, McGill University, Montréal, Canada
3 Department of Mechanical Engineering, Concordia University, Montréal, Quebec, Canada
4 Faculty of Pharmacy, University of Aleppo, Aleppo, Syria

*Author to whom correspondence should be addressed.

Academic Editor: Claudia Andl

Front. Biosci. (Schol Ed) 2012, 4(2), 671–684; https://doi.org/10.2741/S292
Published: 1 January 2012
(This article belongs to the Special Issue E-cadherin function in development and cancer)
Abstract

The epidermal growth factor receptor (EGF-R) signaling pathway maintains a balance between cell proliferation, differentiation and apoptosis, and thus it is believed that EGF-R signaling pathways play an important role in the development and progression of several human carcinomas. Epithelial-mesenchymal transition (EMT) describes the dedifferentiation switch between polarized epithelial cancer cells and contractile and motile mesenchymal (invasive) cells during cancer progression and metastasis. Activation of EGF-R signaling regulates EMT-associated invasion and migration in normal and malignant epithelial cells. In contrast, blocking EGF-R and consequently its pathways, by a monoclonal antibody (mAb) or a tyrosine kinase inhibitor (TKI), inhibit cellular migration and invasion, suggesting an essential role for EGF-R inhibitors in the control of cancer metastasis. The purpose of this review is to summarize current information regarding the role of EGF-R signaling on EMT during human cancer progression and metastasis.

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