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J Biol Chem, Vol. 274, Issue 16, 10911-10915, April 16, 1999
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From the Departments of Oncogenes enhance the expression of
cyclooxygenase (Cox)-2, but interactions between tumor suppressor genes
and Cox-2 have not been studied. In the present work, we have compared
the levels of Cox-2 and the production of prostaglandin
E2 in mouse embryo fibroblasts that do not express
any p53 ((10)1) versus the same cell line ((10.1)Val5)
engineered to overexpress wild-type (wt) p53 at 32 °C or
mutant p53 at 39 °C. Cells expressing wt p53 showed about a 10-fold
decrease in synthesis of prostaglandin E2 compared with those expressing mutant p53. Levels of Cox-2 protein and mRNA
were markedly suppressed by wt p53 but not by mutant p53. Nuclear
run-offs revealed decreased rates of Cox-2 transcription in
cells expressing wt p53. The activity of the Cox-2 promoter was reduced by 85% in cells expressing wt p53 but was reduced only by
30% in cells expressing mutant p53 compared with cells null for p53.
The effect of p53 on the suppression of Cox-2 promoter activity was localized to the first 40 base pairs 5' from the transcription start site. Electrophoretic mobility shift assay revealed
that p53 competed with TATA-binding protein for binding to mouse
Cox-2 or human Cox-2 promoter extending from
Medicine,
§ Surgery, and Cardiothoracic Surgery,
50 to +52 base pairs. The results of this study suggest that
interactions between p53 and Cox-2 could be important for understanding
why levels of Cox-2 are undetectable in normal cells and increased in
many tumors.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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