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Suppression of the Neoplastic Phenotype in Vivo by an Anti-ras Ribozyme¹

Section of Biochemical Pharmacology, Department of Medical Oncology, Montana Building, City of Hope National Medical Center, Duarte, California 91010 [K. J. S.]; Department of Tumor Biology, Institute for Cancer Research, The Norwegian Radium Hospital, Montebello, Oslo, Norway [V. A. E, O. E]; Department of Dermatology, University of California at San Francisco, San Francisco, California 94143 [M. K-S.]; and Department of Clinical and Laboratory Medicine, Tohoku University School of Medicine, Seiryocho-1-1, Aoba-ku, Sendai 980, Japan [T. F.]

² To whom requests for reprints should be addressed.

In this study, the efficacy of an anti-ras ribozyme in reversing the neoplastic phenotype was investigated. Murine NIH3T3 cells were trans-fected with cellular DNA from the FEMX-I human melanoma cell line expressing the activated H-ras gene. The transformed cells displayed the neoplastic phenotype in vitro and were tumorigenic in nude mice in vivo. When the transformants were transfected by a ribozyme designed to cleave only activated H-ras RNA, the transformed phenotype was abrogated. In contrast, expression of a mutant ribozyme, essentially acting only as antisense, into the transformed cells resulted in less dramatic changes in cell growth and tumorigenicity. These results reinforce the potential role of anti-oncogene ribozymes as suppressors of neoplastic growth, with possible implications for gene therapy.

¹ This work was supported by a grant from the NIH (CA 50618) and Gene Shears, Ltd.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 12/ 6/93. Accepted 1/13/94.

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