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[Cancer Research 59, 2297-2301, May 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 2297-2301, May 15, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

D-Type Cyclins Complex with the Androgen Receptor and Inhibit Its Transcriptional Transactivation Ability1

Karen E. Knudsen, Webster K. Cavenee and Karen C. Arden2

Ludwig Institute for Cancer Research [K. E. K., W. K. C., K. C. A.], Department of Medicine [W. K. C., K. C. A.], Center for Molecular Genetics [W. K. C.], and Cancer Center [W. K. C.], University of California at San Diego, La Jolla, California 92093-0660; and University of Cincinnati School of Medicine, Department of Cell Biology, Cincinnati, Ohio 45267-0521 [K. E. K.]

D-type cyclins regulate distinct cellular processes, such as mitotic cell cycle control, differentiation, and transcription. We have previously shown that the D-type cyclins are critical for the androgen-dependent proliferation of prostate cells. Here, we sought to determine whether cyclin D1 directly influences the transactivation potential of the androgen receptor, a transcription factor that strongly influences androgen-dependent proliferation. We found that ligand-mediated transcriptional activation of a physiological target, prostate-specific antigen, by the androgen receptor was inhibited by cyclins D1 and D3. The ability of D-type cyclins to inhibit androgen receptor transactivation was not shared with other cyclins, and cyclin D1 was as effective as dominant negative mutants of the androgen receptor in inhibiting transactivation. This function of cyclin D1 was independent of its role in cell cycle progression and is likely elicited through its ability to form a specific complex with the androgen receptor. These data underscore the various mechanisms through which the androgen receptor is regulated and also point to a negative feedback role for cyclin D1 in controlling androgen-dependent growth.




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Copyright © 1999 by the American Association for Cancer Research.