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Corrigendum Free access | 10.1172/JCI151719

Selective androgen receptor modulators activate the canonical prostate cancer androgen receptor program and repress cancer growth

Michael D. Nyquist, Lisa S. Ang, Alexandra Corella, Ilsa M. Coleman, Michael P. Meers, Anthony J. Christiani, Cordell Pierce, Derek H. Janssens, Hannah E. Meade, Arnab Bose, Lauren Brady, Timothy Howard, Navonil De Sarkar, Sander B. Frank, Ruth F. Dumpit, James T. Dalton, Eva Corey, Stephen R. Plymate, Michael C. Haffner, Elahe A. Mostaghel, and Peter S. Nelson

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Published June 15, 2021 - More info

Published in Volume 131, Issue 12 on June 15, 2021
J Clin Invest. 2021;131(12):e151719. https://doi.org/10.1172/JCI151719.
© 2021 American Society for Clinical Investigation
Published June 15, 2021 - Version history
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Related article:

Selective androgen receptor modulators activate the canonical prostate cancer androgen receptor program and repress cancer growth
Michael D. Nyquist, … , Elahe A. Mostaghel, Peter S. Nelson
Michael D. Nyquist, … , Elahe A. Mostaghel, Peter S. Nelson
Research Article Oncology

Selective androgen receptor modulators activate the canonical prostate cancer androgen receptor program and repress cancer growth

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Abstract

Prostate cancer (PC) is driven by androgen receptor (AR) activity, a master regulator of prostate development and homeostasis. Frontline therapies for metastatic PC deprive the AR of the activating ligands testosterone (T) and dihydrotestosterone (DHT) by limiting their biosynthesis or blocking AR binding. Notably, AR signaling is dichotomous, inducing growth at lower activity levels, while suppressing growth at higher levels. Recent clinical studies have exploited this effect by administration of supraphysiological concentrations of T, resulting in clinical responses and improvements in quality of life. However, the use of T as a therapeutic agent in oncology is limited by poor drug-like properties as well as rapid and variable metabolism. Here, we investigated the antitumor effects of selective AR modulators (SARMs), which are small-molecule nonsteroidal AR agonists developed to treat muscle wasting and cachexia. Several orally administered SARMs activated the AR program in PC models. AR cistromes regulated by steroidal androgens and SARMs were superimposable. Coregulatory proteins including HOXB13 and GRHL2 comprised AR complexes assembled by both androgens and SARMs. At bioavailable concentrations, SARMs repressed MYC oncoprotein expression and inhibited the growth of castration-sensitive and castration-resistant PC in vitro and in vivo. These results support further clinical investigation of SARMs for treating advanced PC.

Authors

Michael D. Nyquist, Lisa S. Ang, Alexandra Corella, Ilsa M. Coleman, Michael P. Meers, Anthony J. Christiani, Cordell Pierce, Derek H. Janssens, Hannah E. Meade, Arnab Bose, Lauren Brady, Timothy Howard, Navonil De Sarkar, Sander B. Frank, Ruth F. Dumpit, James T. Dalton, Eva Corey, Stephen R. Plymate, Michael C. Haffner, Elahe A. Mostaghel, Peter S. Nelson

×

Original citation: J Clin Invest. 2021;131(10):e146777. https://doi.org/10.1172/JCI146777

Citation for this corrigendum: J Clin Invest. 2021;131(12):e151719. https://doi.org/10.1172/JCI151719

The heatmap shown in Figure 2A was incorrect. The correct figure part is below. The manuscript has been corrected online.

The authors regret the error.

Footnotes

See the related article at Selective androgen receptor modulators activate the canonical prostate cancer androgen receptor program and repress cancer growth.

Version history
  • Version 1 (June 15, 2021): Electronic publication

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