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J. Biol. Chem., Vol. 276, Issue 50, 47709-47714, December 14, 2001
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From the Division of Hematology/Oncology, Cedars-Sinai Medical
Center, UCLA School of Medicine, Los Angeles, California 90048 and the
§ Department of Medicine, Hematology and Oncology,
University of Muenster, Muenster 48129, Germany
Cysteine-rich protein 61 (Cyr61) is a
member of a family of growth factor-inducible immediate-early genes. It
regulates cell adhesion, migration, proliferation, and differentiation
and is involved in tumor growth. In our experiments, the role of Cyr61 in non-small cell lung cancer (NSCLC) was examined. Expression of Cyr61
mRNA was decreased markedly in four of five human lung tumor
samples compared with their normal matched lung samples. NSCLC cell
lines NCI-H520 and H460, which have no endogenous Cyr61, formed
60-90% fewer colonies after being transfected with a Cyr61 cDNA
expression vector than cells transfected with the same amount of empty
vector. After stable transfection of a Cyr61 cDNA expression vector, proliferation of both H520-Cyr61 and H460-Cyr61 sublines decreased remarkably compared with the cells stably transfected with
empty vector. The addition of antibody against Cyr61 partially rescued
the growth suppression of both H520-Cyr61 and H460-Cyr61 cells. Cell
cycle analysis revealed that both H520-Cyr61 and H460-Cyr61 cells
developed G1 arrest, prominently up-regulated
expression of p53 and p21WAF1, and had
decreased activity of cyclin-dependent kinase 2. The increase of pocket protein pRB2/p130 was also detected in these cells.
Notably, both of the Cyr61-stably transfected lung cancer cell lines
developed smaller tumors than those formed by the wild-type cells in
nude mice. Taken together, we conclude that Cyr61 may play a role as a
tumor suppressor in NSCLC.
Cyr61, a Member of CCN Family, Is a Tumor Suppressor in Non-Small
Cell Lung Cancer*
,
*
This work was supported by the National Institutes of
Health, the Porka Hugher Fund, Horn Trust, Ko-So Foundation, and the C. and H. Koeffler Fund.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Division of
Hematology/Oncology, Cedars-Sinai Medical Center, Davis Bldg., Rm. 5022, 8700 Beverly Blvd., Los Angeles, CA 90048. Tel.:
310-423-7739; Fax: 310-423-0225, E-mail:
xiangjuntong@hotmail.com.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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