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Title: Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells

Abstract

Normal cells show contact inhibition of cell movement and proliferation, but this is lost following transformation. We found that Necl-5, originally identified as a poliovirus receptor and up-regulated in many cancer cells, enhances growth factor-induced cell movement and proliferation. We showed that when cells contact other cells, Necl-5 interacts in trans with nectin-3 and is removed by endocytosis from the cell surface, resulting in a reduction of cell movement and proliferation. We show here that up-regulation of the gene encoding Necl-5 by the oncogene V12-Ki-Ras causes enhanced cell movement and proliferation. Upon cell-cell contact, de novo synthesis of Necl-5 exceeds the rate of Necl-5 endocytosis, eventually resulting in a net increase in the amount of Necl-5 at the cell surface. In addition, expression of the gene encoding nectin-3 is markedly reduced in transformed cells. Thus, up-regulation of Necl-5 following transformation contributes to the loss of contact inhibition in transformed cells.

Authors:
 [1];  [2];  [1];  [1];  [1];  [2];  [3];  [4]
  1. Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka (Japan)
  2. (Japan)
  3. Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka (Japan)
  4. Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka (Japan). E-mail: ytakai@molbio.med.osaka-u.ac.jp
Publication Date:
OSTI Identifier:
20857972
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 352; Journal Issue: 4; Other Information: DOI: 10.1016/j.bbrc.2006.11.089; PII: S0006-291X(06)02559-9; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANTIBODIES; BIOSYNTHESIS; CELL PROLIFERATION; GENE REGULATION; GROWTH FACTORS; INHIBITION; MOLECULES; NEOPLASMS; ONCOGENES; POLIO VIRUS; POTASSIUM IODIDES; RECEPTORS; RNA

Citation Formats

Minami, Yukiko, Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Ikeda, Wataru, Kajita, Mihoko, Fujito, Tsutomu, Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Monden, Morito, and Takai, Yoshimi. Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells. United States: N. p., 2007. Web. doi:10.1016/j.bbrc.2006.11.089.
Minami, Yukiko, Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Ikeda, Wataru, Kajita, Mihoko, Fujito, Tsutomu, Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Monden, Morito, & Takai, Yoshimi. Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells. United States. doi:10.1016/j.bbrc.2006.11.089.
Minami, Yukiko, Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Ikeda, Wataru, Kajita, Mihoko, Fujito, Tsutomu, Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Monden, Morito, and Takai, Yoshimi. Fri . "Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells". United States. doi:10.1016/j.bbrc.2006.11.089.
@article{osti_20857972,
title = {Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells},
author = {Minami, Yukiko and Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka and Ikeda, Wataru and Kajita, Mihoko and Fujito, Tsutomu and Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka and Monden, Morito and Takai, Yoshimi},
abstractNote = {Normal cells show contact inhibition of cell movement and proliferation, but this is lost following transformation. We found that Necl-5, originally identified as a poliovirus receptor and up-regulated in many cancer cells, enhances growth factor-induced cell movement and proliferation. We showed that when cells contact other cells, Necl-5 interacts in trans with nectin-3 and is removed by endocytosis from the cell surface, resulting in a reduction of cell movement and proliferation. We show here that up-regulation of the gene encoding Necl-5 by the oncogene V12-Ki-Ras causes enhanced cell movement and proliferation. Upon cell-cell contact, de novo synthesis of Necl-5 exceeds the rate of Necl-5 endocytosis, eventually resulting in a net increase in the amount of Necl-5 at the cell surface. In addition, expression of the gene encoding nectin-3 is markedly reduced in transformed cells. Thus, up-regulation of Necl-5 following transformation contributes to the loss of contact inhibition in transformed cells.},
doi = {10.1016/j.bbrc.2006.11.089},
journal = {Biochemical and Biophysical Research Communications},
number = 4,
volume = 352,
place = {United States},
year = {Fri Jan 26 00:00:00 EST 2007},
month = {Fri Jan 26 00:00:00 EST 2007}
}