Home  |   Archive  |   Online Submission  |   News & Events  |   Subscribe  |   APFA  |   Society  |   Contact Us  |   中文版

Ahead of print
Authors' Accepted
Current Issue
Special Issues
Browse by Category

Manuscript Submission

Online Submission
Online Review
Instruction for Authors
Instruction for Reviewers
English Corner new!

About AJA

About AJA
Editorial Board
Contact Us

Resources & Services

Email alert

Download area

Copyright licence
EndNote style file
Manuscript word template
Guidance for AJA figures
    preparation (in English)

Guidance for AJA figures
    preparation (in Chinese)

Proof-reading for the

AJA Club (in English)
AJA Club (in Chinese)


Volume 15, Issue 4 (July 2013) 15, 447–448; 10.1038/aja.2013.62

The ubiquitin ligase Siah2 is revealed as an accomplice of the androgen receptor in castration resistant prostate cancer

Michael R Freeman

Research Division of Cancer Biology and Therapeutics, Departments of Surgery, Medicine and Biomedical Sciences, Cancer Biology Program, Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA 90048, USA

Correspondence: Dr MR Freeman, (Michael.freeman@cshs.org)

advance online publication, May 27, 2013


The androgen receptor (AR) remains the primary molecular target for prostate cancer (PCa) treatment and for development of novel therapies. Profiling and other analyses of human prostate adenocarcinoma have shown that the AR is still functional during late-stage disease in the absence of circulating hormone following castration therapy. The molecular mechanisms that operate during this ‘castration resistant’ phase are still not well understood. Qi et al. have now implicated the ubiquitin ligase Siah2 as an important mediator of AR action in castration resistant prostate cancer (CRPC). Siah2 was found to target repressed AR chromatin complexes for degradation, resulting in activation of AR-regulated genes involved in tumor cell proliferation, cell motility and lipid metabolism. The authors show a requirement for Siah2 activity for PCa cell growth under conditions of low androgen, and also that targeting Siah2 results in tumor growth suppression under castrate conditions. These findings identify a new mechanism of AR regulation in progressing disease as well as a novel enzymatic target for therapeutic intervention.


Browse:  3007
Asian Journal of Andrology CN 31-1795/R ISSN 1008-682X  Copyright © 2023  Shanghai Materia Medica, Chinese Academy of Sciences.  All rights reserved.