Abstract
Cells induced to accumulate the p53 tumor suppressor protein have been shown to arrest in G1. This arrest is characterized by accumulation of the cyclin-dependent kinase inhibitor p21 (WAF1/CIP1) and of underphosphorylated forms of retinoblastoma protein. We show here that accumulation of the wild-type p53 protein in either human or murine cells markedly increases expression of cyclin D1. The induction of cyclin D1 can also be mediated by a target of p53, the p21 (WAF1/CIP1) inhibitor of cyclin-dependent kinases. The relationship between the induction of cyclin D1 and G1 arrest defines a new cellular response to p53.
Footnotes
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↵1 This work was supported by a grant from U.S. Army breast cancer program (DAMD17-94-J-4275 to C. P.) X. C. was supported by a postdoctoral fellowship from the U.S. Army breast cancer program (DAMD17-94-J-4142).
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↵2 To whom requests for reprints should be addressed.
- Received June 29, 1995.
- Accepted August 18, 1995.
- ©1995 American Association for Cancer Research.
Volume 55, Issue 19
