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Department of Radiation Oncology [T. C. T., L. M-T., J. K., G. T. B.], College of Medicine, University of Arizona, Tucson, Arizona 85724, Department of Anatomy [M. J. C. H.], College of Medicine, University of Arizona, Tucson, Arizona 85724, Department of Medicine, College of Medicine [M. B. P.], University of Arizona, Tucson, Arizona 85724, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan, Republic of China [Y-W. C.]
2 To whom requests for reprints should be addressed, at Department of Radiation Oncology, College of Medicine, University of Arizona, 1501 N. Campbell Ave., Tucson, AZ 85724.
The viral jun (v-jun) oncogene encodes a transcription factor that can participate in the transactivation of genes through the AP-1 complex. Evidence indicates that the ability of v-jun to transform cells and stimulate transcription depends on the cell type. We have asked whether expression of the v-jun gene in benign tumor forming mouse keratinocytes that already express an activated c-rasHa oncogene would cause malignant progression. Our results showed that the v-jun transfection did not result in malignant progression; instead, we made the unexpected observation that the ability of these cells to invade reconstituted basement membrane matrix (in vitro) in response to the phorbol ester, 12-O-tetradecanoylphor-bol-13-acetate, was suppressed. This phenomenon could, in part, be explained by the suppression of the induction by phorbol ester of expression of the metalloproteinase, stromelysin (transin). Of interest was the finding that 12-O-tetradecanoylphorbol-13-acetate induction of other cellular genes known to be regulated by AP-1 was not inhibited in the benign tumor cells expressing v-jun.
1 Supported in part by USPHS Grants CA-40584 (to G. T. B.) and CA-51971 (to M. B. P.).
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 10/20/93. Accepted 1/ 4/94.
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