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Molecular and Cellular Biology, October 2007, p. 7125-7142, Vol. 27, No. 20
0270-7306/07/$08.00+0     doi:10.1128/MCB.01753-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Cyclin D3/CDK11p58 Complex Is Involved in the Repression of Androgen Receptor{triangledown}

Hongliang Zong,1 Yayun Chi,1 Yanlin Wang,1 Yanzhong Yang,1 Li Zhang,2 Haijiao Chen,2 Jianhai Jiang,1 Zejuan Li,1 Yi Hong,1 Hanzhou Wang,1 Xiaojing Yun,1 and Jianxin Gu1*

Key Laboratory of Medical Molecular Virology, Ministry of Education and Health, Gene Research Center, Shanghai Medical College and Institutes of Biomedical Sciences,1 Department of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China2

Received 16 September 2006/ Returned for modification 20 October 2006/ Accepted 26 July 2007

Androgen receptor (AR) is essential for the maintenance of the male reproductive systems and is critical for the carcinogenesis of human prostate cancers (PCas). D-type cyclins are closely related to the repression of AR function. It has been well documented that cyclin D1 inhibits AR function through multiple mechanisms, but the mechanism of how cyclin D3 exerts its repressive role in the AR signaling pathway remains to be identified. In the present investigation, we demonstrate that cyclin D3 and the 58-kDa isoform of cyclin-dependent kinase 11 (CDK11p58) repressed AR transcriptional activity as measured by reporter assays of transformed cells and prostate-specific antigen expression in PCa cells. AR, cyclin D3, and CDK11p58 formed a ternary complex in cells and were colocalized in the luminal epithelial layer of the prostate. AR activity is controlled by phosphorylation at specific sites. We found that AR was phosphorylated at Ser-308 by cyclin D3/CDK11p58 in vitro and in vivo, leading to the repressed activity of AR transcriptional activation unit 1 (TAU1). Furthermore, androgen-dependent proliferation of PCa cells was inhibited by cyclin D3/CDK11p58 through AR repression. These data suggest that cyclin D3/CDK11p58 signaling is involved in the negative regulation of AR function.

* Corresponding author. Mailing address: Box 103, No. 138 Yi Xue Yuan Road, Gene Research Center, Shanghai Medical College of Fudan University, Shanghai 200032, People's Republic of China. Phone: 86-21-54237704. Fax: 86-21-64164489. E-mail: jxgu{at}shmu.edu.cn

{triangledown} Published ahead of print on 13 August 2007.

Molecular and Cellular Biology, October 2007, p. 7125-7142, Vol. 27, No. 20
0270-7306/07/$08.00+0     doi:10.1128/MCB.01753-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Kong, X., Gan, H., Hao, Y., Cheng, C., Jiang, J., Hong, Y., Yang, J., Zhu, H., Chi, Y., Yun, X., Gu, J. (2009). CDK11p58 Phosphorylation of PAK1 Ser174 Promotes DLC2 Binding and Roles on Cell Cycle Progression. J Biochem 146: 417-427 [Abstract] [Full Text]  
  • Wang, Y., Zong, H., Chi, Y., Hong, Y., Yang, Y., Zou, W., Yun, X., Gu, J. (2009). Repression of Estrogen Receptor alpha by CDK11p58 Through Promoting its Ubiquitin-Proteasome Degradation. J Biochem 145: 331-343 [Abstract] [Full Text]  
  • Loyer, P., Trembley, J. H., Grenet, J. A., Busson, A., Corlu, A., Zhao, W., Kocak, M., Kidd, V. J., Lahti, J. M. (2008). Characterization of Cyclin L1 and L2 Interactions with CDK11 and Splicing Factors: INFLUENCE OF CYCLIN L ISOFORMS ON SPLICE SITE SELECTION. J. Biol. Chem. 283: 7721-7732 [Abstract] [Full Text]  


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