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Originally published In Press as doi:10.1074/jbc.M107878200 on October 11, 2001

J. Biol. Chem., Vol. 276, Issue 50, 47709-47714, December 14, 2001
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Cyr61, a Member of CCN Family, Is a Tumor Suppressor in Non-Small Cell Lung Cancer*

Xiangjun TongDagger , Dong Xie, James O'Kelly, Carl W. Miller, Carsten Muller-Tidow§, and H. Phillip Koeffler

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.

* 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.

Dagger 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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