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Molecular and Cellular Biology, October 1998, p. 6131-6141, Vol. 18, No. 10
Vanderbilt Cancer Center, Department of Cell
Biology, Vanderbilt University, Nashville, Tennessee
37232,1 and
Division of Cell Growth and
Regulation, Dana-Farber Cancer Institute, Boston, Massachusetts
021152
Received 22 January 1998/Returned for modification 2 March
1998/Accepted 20 July 1998
By using a model system for cell transformation mediated by the
cooperation of the activated H-ras oncogene and the
inactivated p53 tumor suppressor gene, rCop-1 was
identified by mRNA differential display as a gene whose expression
became lost after cell transformation. Homology analysis indicates that
rCop-1 belongs to an emerging cysteine-rich growth regulator family
called CCN, which includes connective-tissue growth factor, CYR61,
CEF10 (v-src inducible), and the product of the
nov proto-oncogene. Unlike the other members of the CCN
gene family, rCop-1 is not an immediate-early gene, it
lacks the conserved C-terminal domain which was shown to confer both
growth-stimulating and heparin-binding activities, and its expression
is lost in cells transformed by a variety of mechanisms. Ectopic
expression of rCop-1 by retroviral gene transfers led to
cell death in a transformation-specific manner. These results suggest
that rCop-1 represents a new class of CCN family proteins that have
functions opposing those of the previously identified members.
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Identification of rCop-1, a New Member of the CCN
Protein Family, as a Negative Regulator for Cell
Transformation
*
Corresponding author. Mailing address: Vanderbilt
Cancer Center, Department of Cell Biology, Vanderbilt University, 658 Medical Research Building II, Nashville, TN 37232. Phone: (615)
936-2182. Fax: (615) 936-2183. E-mail:
peng.liang{at}mcmail.vanderbilt.edu.
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