Target cell movement in tumor and cardiovascular diseases based on the epithelial-mesenchymal transition concept.

Adv Drug Deliv Rev

Institute of Molecular Cell Biology, Experimental Therapeutic Centre, Biopolis A*STAR, Cancer Science Institute National University of Singapore and Department of Obstetrics and Gynaecology, National University Hospital, Singapore, Republic of Singapore.

Published: July 2011

AI Article Synopsis

  • Epithelial-mesenchymal transition (EMT) is a key developmental process where epithelial cells change to a mesenchymal phenotype, altering their behavior to enable migration and invasion.
  • EMT allows carcinoma cells to metastasize and gain resistance against treatments, while also playing roles in heart regeneration and fibrosis.
  • Research into EMT may lead to new therapies targeting cell movement for treating cancer and cardiovascular diseases.

Article 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.

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Source
http://dx.doi.org/10.1016/j.addr.2011.02.003DOI Listing

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