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Molecular and Cellular Biology, March 2006, p. 1908-1916, Vol. 26, No. 5
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.5.1908-1916.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Androgen and Its Receptor Promote Bax-Mediated Apoptosis{dagger}

Yuting Lin,1,2 John Kokontis,3 Fangming Tang,3 Bradley Godfrey,1 Shutsung Liao,3 Anning Lin,3 Youting Chen,2 and Jialing Xiang1*

Department of Biological, Chemical, and Physical Science, Illinois Institute of Technology, Chicago, Illinois 60616,1 Department of Neurobiology, Xuzhou Medical College, Xuzhou 221002, People's Republic of China,2 Ben May Institute for Cancer Research, The University of Chicago, Chicago, Illinois 606373

Received 18 April 2005/ Returned for modification 11 June 2005/ Accepted 11 November 2005

Androgen and its receptor (AR) have been reported to have pro- or antiapoptotic functions. However, the underlying molecular mechanism is incompletely understood. We report here that androgen and AR promote Bax-mediated apoptosis in prostate cancer cells. UV irradiation and ectopic expression of Bax induce apoptosis in AR-positive, but not AR-negative prostate cancer cells. UV- and Bax-induced apoptosis is abrogated in AR-positive cells that express small interference RNA (siRNA) of AR and is sensitized by reintroduction of AR into AR-negative cells. Although AR is able to promote Bax-mediated apoptosis independently of androgen, the promotion by AR can be further potentiated by androgen via AR-dependent transcription activation. AR is essential for the translocation of Bax to mitochondria in UV- or Bax-induced apoptosis. Inhibition of Bax expression by Bax siRNA suppresses UV-induced apoptosis in AR-positive cells. In addition, introduction of AR into AR-negative prostate cancer cells upregulates expression levels of the BH3-only protein Noxa, whereas inhibition of Noxa expression reduces the promotion by AR on UV-induced apoptosis. Thus, our results reveal a novel cross talk between the androgen/AR hormonal signaling pathway and the intrinsic apoptotic death pathway that determines the sensitivity of stress-induced apoptosis in prostate cancer cells.

* Corresponding author. Mailing address: Department of Biological, Chemical, and Physical Science, Illinois Institute of Technology, Chicago, IL 60616. Phone: (312) 567-3491. Fax: (312) 567-3494. E-mail: xiang{at}iit.edu.

{dagger} This study is dedicated in memory of Jialing Xiang's mentor, Stanley Korsmeyer, who passed away due to lung cancer on 31 March 2005.

Molecular and Cellular Biology, March 2006, p. 1908-1916, Vol. 26, No. 5
0022-538X/06/$08.00+0     doi:10.1128/MCB.26.5.1908-1916.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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