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

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 th...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2007-01, Vol.352 (4), p.856-860
Main Authors: Minami, Yukiko, Ikeda, Wataru, Kajita, Mihoko, Fujito, Tsutomu, Monden, Morito, Takai, Yoshimi
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
ANTIBODIES
BIOSYNTHESIS
CD155
Cell Adhesion Molecules - metabolism
Cell movement
CELL PROLIFERATION
Contact inhibition
Endocytosis
GENE REGULATION
GROWTH FACTORS
INHIBITION
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice
MOLECULES
Necl-5
Nectin
Nectins
NEOPLASMS
NIH 3T3 Cells
ONCOGENES
POLIO VIRUS
Poliovirus
Poliovirus receptor
POTASSIUM IODIDES
Protein Binding
Ras
ras Proteins - genetics
ras Proteins - metabolism
RECEPTORS
Receptors, Virus - genetics
Receptors, Virus - metabolism
RNA
Tage4
Transformation
Transformation, Genetic - genetics
Up-Regulation
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Summary: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.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2006.11.089