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© The Rockefeller University Press, 0021-9525/2000//873 $5.00
The Journal of Cell Biology, Volume 150, Number 4, , 2000 873-880

Cyclin E as a Coactivator of the Androgen Receptor

^a Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113, Japan
^b Department of Geriatric Research, National Institute for Longevity Sciences, Obu, Aichi 474-8522, Japan
^c Department of Urology, Nagoya City University Medical School, Nagoya 467-8601, Japan
^d Department of Biochemistry, Nagoya City University Medical School, Nagoya 467-8601, Japan
^e Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo 170-8455, Japan
^f CREST, Japan Science and Technology Corporation, Saitama 332, Japan
Department of Biochemistry, Nagoya City University Medical School, Kawasumi 1, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan.+81-52-842-3955+81-52-853-8145

mkt-naka{at}med.nagoya-cu.ac.jp

Androgens play an important role in the growth of prostate cancer, but the molecular mechanism that underlies development of resistance to antiandrogen therapy remains unknown. Cyclin E has now been shown to increase the transactivation activity of the human androgen receptor (AR) in the presence of its ligand dihydrotestosterone. The enhancement of AR activity by cyclin E was resistant to inhibition by the antiandrogen 5-hydroxyflutamide. Cyclin E was shown to bind directly to the COOH terminus portion of the AB domain of the AR, and to enhance its AF-1 transactivation function. These results suggest that cyclin E functions as a coactivator of the AR, and that aberrant expression of cyclin E in tumors may contribute to persistent activation of AR function, even during androgen ablation therapy.

Key Words: cyclin E • androgen receptor • prostate cancer • coactivator • cell cycle

© 2000 The Rockefeller University Press

Abbreviations used in this paper: AR, androgen receptor; ARE, androgen response element; CAT, chloramphenicol acetyltransferase; Cdk, cyclin-dependent kinase; DBD, DNA-binding domain; DHT, dihydrotestosterone; ER, estrogen receptor ; GR, glucocorticoid receptor; GST, glutathione S-transferase; 5-OH-F, 5-hydroxyflutamide; PR, progesterone receptor; PSA, prostate-specific antigen.

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