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.
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10 October 2005
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October 10 2005
Inhibition of cell movement and proliferation by cell–cell contact-induced interaction of Necl-5 with nectin-3
Tsutomu Fujito,
Tsutomu Fujito
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
2Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
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Wataru Ikeda,
Wataru Ikeda
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
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Shigeki Kakunaga,
Shigeki Kakunaga
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
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Yukiko Minami,
Yukiko Minami
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
2Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
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Mihoko Kajita,
Mihoko Kajita
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
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Yasuhisa Sakamoto,
Yasuhisa Sakamoto
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
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Morito Monden,
Morito Monden
2Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
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Yoshimi Takai
Yoshimi Takai
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
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Tsutomu Fujito
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
2Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
Wataru Ikeda
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
Shigeki Kakunaga
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
Yukiko Minami
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
2Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
Mihoko Kajita
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
Yasuhisa Sakamoto
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
Morito Monden
2Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
Yoshimi Takai
1Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan
Correspondence to Yoshimi Takai: [email protected]
Abbreviations used in this paper: Ab, antibody; DN, dominant-negative; MEF, mouse embryonic fibroblast; pAb, polyclonal Ab; PVR, poliovirus receptor; siRNA, small interfering RNA.
Received:
January 18 2005
Accepted:
September 02 2005
Online ISSN: 1540-8140
Print ISSN: 0021-9525
The Rockefeller University Press
2005
J Cell Biol (2005) 171 (1): 165–173.
Article history
Received:
January 18 2005
Accepted:
September 02 2005
Connected Content
This article has been corrected
Correction: Inhibition of cell movement and proliferation by cell–cell contact-induced interaction of Necl-5 with nectin-3
Citation
Tsutomu Fujito, Wataru Ikeda, Shigeki Kakunaga, Yukiko Minami, Mihoko Kajita, Yasuhisa Sakamoto, Morito Monden, Yoshimi Takai; Inhibition of cell movement and proliferation by cell–cell contact-induced interaction of Necl-5 with nectin-3 . J Cell Biol 10 October 2005; 171 (1): 165–173. doi: https://doi.org/10.1083/jcb.200501090
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