2007年1月
Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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- 巻
- 352
- 号
- 4
- 開始ページ
- 856
- 終了ページ
- 860
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/j.bbrc.2006.11.089
- 出版者・発行元
- ACADEMIC PRESS INC ELSEVIER SCIENCE
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. (c) 2006 Elsevier Inc. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/j.bbrc.2006.11.089
- ISSN : 0006-291X
- Web of Science ID : WOS:000243317100005