[Frontiers in Bioscience S4, 671-684, January 1, 2012]

EGF-receptor signaling and epithelial-mesenchymal transition in human carcinomas

Ala-Eddin Al Moustafa1 ,2 ,3, Amal Achkhar1, 4, Amber Yasmeen2

1Syrian Research Cancer Centre of the Syrian Society against Cancer, Aleppo, Syria, Oncology Department, Faculty of Medicine, McGill University, Montréal, Canada; Department of Mechanical Engineering, Concordia University, Montréal, Quebec, Canada; 4Faculty of Pharmacy, University of Aleppo, Aleppo, Syria

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Epidermal growth factor receptor signaling
4. Epithelial-mesenchymal transition and E-cadherin expression
5. Epithelial-mesenchymal transition/Epidermal growth factor receptor interaction
6. Conclusions and Future Perspectives
7. Acknowledgments
8. References

1. 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.