Document Detail


Involvement of up-regulated Necl-5/Tage4/PVR/CD155 in the loss of contact inhibition in transformed NIH3T3 cells.
MedLine Citation:
PMID:  17156749     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Yukiko Minami; Wataru Ikeda; Mihoko Kajita; Tsutomu Fujito; Morito Monden; Yoshimi Takai
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-11-29
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  352     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2007 Jan 
Date Detail:
Created Date:  2006-12-18     Completed Date:  2007-03-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  856-60     Citation Subset:  IM    
Affiliation:
Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Suita 565-0871, Osaka, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Adhesion Molecules / metabolism
Endocytosis
Membrane Proteins / genetics,  metabolism*
Mice
NIH 3T3 Cells
Protein Binding
Receptors, Virus / genetics,  metabolism*
Transformation, Genetic / genetics*
Up-Regulation*
ras Proteins / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Cell Adhesion Molecules; 0/Membrane Proteins; 0/Receptors, Virus; 0/nectins; 0/poliovirus receptor; EC 3.6.5.2/ras Proteins

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