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Title 

Tetraspanin TM4SF5 mediates loss of contact inhibition through epithelial-mesenchymal transition in human hepatocarcinoma

Authors 

S A LeeS Y LeeI H ChoM A OhE S KangY B KimW D SeoS ChoiJ O NamM Tamamori-AdachiS KitajimaS K YeSemi KimY J HwangI S KimK H ParkJ W Lee

Publisher 

American Society for Clinical Investigation

Issue Date 

2008

Citation 

Journal of Clinical Investigation, vol. 118, no. 4, pp. 1354-1366

Keywords 

protein TM4SF5tetraspanincontact inhibitionhumanhuman cellcontact Inhibitionepithelial cellshumans

Abstract 

The growth of normal cells is arrested when they come in contact with each other, a process known as contact inhibition. Contact inhibition is lost during tumorigenesis, resulting in uncontrolled cell growth. Here, we investigated the role of the tetraspanin transmembrane 4 superfamily member 5 (TM4SF5) in contact inhibition and tumorigenesis. We found that TM4SF5 was overexpressed in human hepatocarcinoma tissue. TM4SF5 expression in clinical samples and in human hepatocellular carcinoma cell lines correlated with enhanced p27Kip1 expression and cytosolic stabilization as well as morphological elongation mediated by RhoA inactivation. These TM4SF5-mediated effects resulted in epithelial-mesenchymal transition (EMT) via loss of E-cadherin expression. The consequence of this was aberrant cell growth, as assessed by S-phase transition in confluent conditions, anchorage-independent growth, and tumor formation in nude mice. The TM4SF5-mediated effects were abolished by suppressing the expression of either TM4SF5 or cytosolic p27Kip1, as well as by reconstituting the expression of E-cadherin. Our observations have revealed a role for TM4SF5 in causing uncontrolled growth of human hepatocarcinoma cells through EMT.

ISSN 

0021-9738

Link 

http://dx.doi.org/10.1172/JCI33768

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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