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Published 10 October 2005. doi:10.1083/jcb.200501090
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 171, Number 1, 165-173
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Article

 Inhibition of cell movement and proliferation by cell–cell contact-induced interaction of Necl-5 with nectin-3

Tsutomu Fujito1,2, Wataru Ikeda1, Shigeki Kakunaga1, Yukiko Minami1,2, Mihoko Kajita1, Yasuhisa Sakamoto1, Morito Monden2, and Yoshimi Takai1

1 Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
2 Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan

Correspondence to Yoshimi Takai: ytakai{at}molbio.med.osaka-u.ac.jp

Immunoglobulin-like Necl-5/Tage4/poliovirus receptor (PVR)/CD155, originally identified as the PVR, has been shown to be up-regulated in cancer cells and to enhance growth factor–induced cell movement and proliferation. In addition, Necl-5 heterophilically trans-interacts with nectin-3, a cell–cell adhesion molecule known to form adherens junctions in cooperation with cadherin. We show here that Necl-5 was down-regulated from cell surface upon cell–cell contacts in NIH3T3 cells. This down-regulation of Necl-5 was initiated by its interaction with nectin-3 and was mainly mediated by clathrin-dependent endocytosis. Then, the down-regulation of Necl-5 induced in this way reduced movement and proliferation of NIH3T3 cells. These results indicate that the down-regulation of Necl-5 induced by its interaction with nectin-3 upon cell–cell contacts may be at least one mechanism underlying contact inhibition of cell movement and proliferation.

Abbreviations used in this paper: Ab, antibody; DN, dominant-negative; MEF, mouse embryonic fibroblast; pAb, polyclonal Ab; PVR, poliovirus receptor; siRNA, small interfering RNA.


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