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Wild-type but not Mutant p53 Suppresses the Growth of Human Lung Cancer Cells Bearing Multiple Genetic Lesions¹

Laboratories of Chemotherapy [Ta. T., R. U.] and Immunology [To. T.], Aichi Cancer Center Research Institute, Chikusa-ku, Nagoya 464, Japan; Department of Internal Medicine, Aichi Cancer Center Hospital, Chikusa-ku, Nagoya 464, Japan [T. H.]; NCI-Navy Medical Oncology Branch, National Cancer Institute, Bethesda, Maryland 20814 [M. M. N., I. L.]; and Harold Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas 75235 [D. C., J. D. M.]

Accumulating evidence indicates that lung cancer arises due to multiple genetic changes in both dominant oncogenes, such as ras, and tumor suppressor genes, such as p53. In this report we examined whether the wild-type p53 gene is able to suppress in vitro and/or in vivo cellular growth of lung cancer cell lines which carry multiple genetic abnormalities. Introduction of a wild-type p53 complementary DNA expression vector into lung cancer cell lines carrying either a homozygous deletion (NCI-H358) or a missense mutation (NCI-H23) in the p53 gene greatly suppressed tumor cell growth. In contrast, p53 expression vectors bearing lung cancer derived mutations affecting single amino acids had lost this growth suppressing ability.

¹ This work was supported in part by a Grant-in-Aid for the Comprehensive Ten-Year Strategy for Cancer Research from the Ministry of Health and Welfare, Japan; Grant-in-Aids for Cancer Research from the Ministry of Education, Science, and Culture and the Ministry of Health and Welfare, Japan; and by a grant from the Cancer Research Institute, Inc., New York.

² To whom requests for reprints should be addressed.

Received 1/21/92. Accepted 3/ 4/92.

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