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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2010) 34, S7 (Printed in Great Britain)
Meeting Abstract
Involvement of cystic fibrosis transmembrane conductance regulator (CFTR) in epithelial-mesenchymal transition during cancer development
Jie Ting Zhang, Chin Man Chung and Hsiao Chang Chan
Epithelial Cell Biology Research Center, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong

Epithelial-Mesenchymal Transition (EMT) is an intricate process by which epithelial cells lose their epithelial characteristics, like loss of tight junctions, and acquire a mesenchymal-like phenotype. It is essential for numerous developmental processes. Cancer cells have also been described to undergo EMT acquiring a more invasive and metastatic phenotype. The reverse process, known as mesenchymal-to-epithelial transition (MET), is also involved in the formation of a secondary metastatic tumor. Cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated Cl- channel, which is expressed in epithelial cells of various organs. To investigate the role of CFTR in EMT during cancer metastasis, we employed a highly differentiated colorectal cancer cell line LIM1863. Using this cell model, we report that the expression of CFTR was down regulated in cells undergoing EMT and the down regulation was reversed during MET. In addition, a specific CFTR inhibitor CFTRinh-172 could induce EMT in a dose-dependent manner in LIM 1863. On the contrary, MET was blocked by CFTRinh-172 at similar concentrations. These results suggest that functional CFTR is required for cells to keep epithelial phenotype. Further studies demonstrated expression of actived urokinase-type plasminogen activator (uPA) and uPA-receptor were increased in LIM1863 with CFTRinh-172 treatment, which revealed that CFTR may regulate the processes of EMT through activating uPA/uPAR system.

Published online 1 August 2010, doi:10.1042/CBI034S007a

© The Author(s) Journal compilation © 2010 Portland Press Limited

ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)