Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.addr.2011.02.003
Title: Target cell movement in tumor and cardiovascular diseases based on the epithelial-mesenchymal transition concept
Authors: Chua, K.-N.
Poon, K.L.
Lim, J.
Sim, W.-J.
Huang, R.Y.J.
Thiery, J.P. 
Keywords: Carcinoma
Coronary disease
Epithelial-mesenchymal transition
Fibrosis
Heart
Invasion
Metastasis
Regeneration
Issue Date: 18-Jul-2011
Citation: Chua, K.-N., Poon, K.L., Lim, J., Sim, W.-J., Huang, R.Y.J., Thiery, J.P. (2011-07-18). Target cell movement in tumor and cardiovascular diseases based on the epithelial-mesenchymal transition concept. Advanced Drug Delivery Reviews 63 (8) : 558-567. ScholarBank@NUS Repository. https://doi.org/10.1016/j.addr.2011.02.003
Abstract: Epithelial-mesenchymal transition (EMT) is a fundamental mechanism in development driving body plan formation. EMT describes a transition process wherein polarized epithelial cells lose their characteristics and acquire a mesenchymal phenotype. The apico-basal polarity of epithelial cells is replaced by a front-rear polarity in mesenchymal cells which favor cell-extracellular matrix than intercellular adhesion. These events serve as a prerequisite to the context-dependent migratory and invasive functions of mesenchymal cells. In solid tumors, carcinoma cells undergoing EMT not only invade and metastasize but also exhibit cancer stem cell-like properties, providing resistance to conventional and targeted therapies. In cardiovascular systems, epicardial cells engaged in EMT contribute to myocardial regeneration. Conversely, cardiovascular endothelial cells undergoing EMT cause cardiac fibrosis. Growing evidence has shed light on the potential development of novel therapeutics that target cell movement by applying the EMT concept, and this may provide new therapeutic strategies for the treatment of cancer and heart diseases. © 2011 Elsevier B.V.
Source Title: Advanced Drug Delivery Reviews
URI: http://scholarbank.nus.edu.sg/handle/10635/116893
ISSN: 0169409X
DOI: 10.1016/j.addr.2011.02.003
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