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Vol. 273, Issue 4, 1998-2007, January 23, 1998
From the Department of Molecular and Cell Biology and The Cancer
Research Laboratory, University of California,
Berkeley, California 94720
Glucocorticoids can induce a G1
arrest in the cell cycle progression of BDS1 rat hepatoma cells. In
these cells, dexamethasone, a synthetic glucocorticoid, stimulated a
rapid and selective increase in expression of the p21
cyclin-dependent kinase (CDK) inhibitor mRNA and
protein and virtually abolished CDK2 phosphorylation of the
retinoblastoma protein. Expression of the p27 CDK inhibitor, and other
G1-acting cell cycle proteins, remained unaffected. Dexamethasone stimulated p21 promoter activity in a p53-independent manner that required functional glucocorticoid receptors. Transforming growth factor-
Glucocorticoids Stimulate p21 Gene Expression by Targeting
Multiple Transcriptional Elements within a Steroid Responsive Region of
the p21waf1/cip1 Promoter in Rat Hepatoma Cells
, which also induced a G1 cell cycle
arrest of the hepatoma cells, failed to elicit this response. Analysis
of 5
deletions of the p21 promoter uncovered a glucocorticoid
responsive region between nucleotides 
1481 and 1184, which does not
contain a canonical glucocorticoid response element but which can
confer dexamethasone responsiveness to a heterologous promoter. Fine mapping of this region uncovered three distinct 50-60-base pair transcriptional elements that likely function as targets of
glucocorticoid receptor signaling. Finally, ectopic expression of p21
had no effect on hepatoma cell growth in the absence of glucocorticoids but facilitated the ability of dexamethasone to inhibit cell
proliferation. Thus, our results have established a direct
transcriptional link between glucocorticoid receptor signaling and the
regulated promoter activity of a CDK inhibitor gene that is involved in
the cell cycle arrest of hepatoma cells.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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