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Departments of Internal Medicine [J. A. M., J. D., M. S.] and Molecular Biology and Genetics [J. A. M.], Wayne State University School of Medicine, Detroit, Michigan 48201, and Dallas VA Medical Center and University of Texas Southwestern Medical Center [G. D. L.], Dallas, Texas 75216
Ornithine decarboxylase (ODC) plays a rate-limiting role in polyamine biosynthesis and is intimately associated with cell proliferation and function. Although elevated levels of ODC mRNA, protein, and enzyme activity are consistently detected in transformed cells and tumors, the question remains as to whether ODC gene overexpression has a causative role in tumorigenesis. We have stably transfected NIH/3T3 fibroblasts with an expression construct containing human ODC complementary DNA under transcriptional control of the human ß-actin promoter. Cells transfected with the ß-actin/ODC DNA construct, designated NODC cells, and control transfectants, termed NLK cells, were analyzed for ODC gene expression and cell growth characteristics. ODC activity and mRNA levels were elevated 3–6-fold in NODC cells relative to NLK cells. NODC cells, in contrast to NLK control cells, are not contact inhibited, exhibit anchorage-independent growth, cycle more rapidly, and induce tumors in nude mice more efficiently and rapidly. These results directly establish a causative role for the misregulation of ODC gene expression in the acquisition of a transformation phenotype and provide a model to examine the interaction of ODC and other gene products in neoplastic development.
1 This work was supported by Grant CA-51206 from the National Cancer Institute and by Grant IN-162 from the American Cancer Society.
2 To whom requests for reprints should be addressed.
Received 12/ 8/92. Accepted 3/26/93.
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