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

doi:10.1016/j.bbrc.2006.11.089

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

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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:

Minami, Yukiko ^[1]; Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka ^[2]; Ikeda, Wataru ^[1]; Kajita, Mihoko ^[1]; Fujito, Tsutomu ^[1]; Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka ^[2]; Monden, Morito ^[3]; Takai, Yoshimi ^[4]

Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka (Japan)
(Japan)
Department of Surgery and Clinical Oncology, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka (Japan)
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:: Fri Jan 26 00:00:00 EST 2007

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.

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                    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.

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                    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.

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@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}

}

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DOI: 10.1016/j.bbrc.2006.11.089

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