» Articles » PMID: 20228873

Androgen Receptor Abnormalities in Castration-recurrent Prostate Cancer

Overview
Specialty Endocrinology
Date 2010 Mar 16
PMID 20228873
Citations 18
Authors
Affiliations
Soon will be listed here.
Abstract

The androgen receptor (AR) plays a critical role in prostate cancer (PCa) development and progression. Despite the success of androgen-deprivation therapy, remission occurs in almost all cases. This stage of the disease is called castration-recurrent PCa (CRPC). CRPC cells adapt to low circulating levels of androgens, and active AR is maintained by numerous cellular mechanisms. Some mutations in the AR make it more responsive to lower androgen levels or other steroids. Furthermore, in this advance stage of the disease, PCa cells express the enzymes necessary for de novo synthesis of androgens. AR is also activated in a ligand-independent manner. Therefore, it is important to understand the mechanisms of AR activation and its deregulation during CRPC. The purpose of this article is to discuss mechanisms that are involved in modulation of AR activity and specificity.

Citing Articles

Reduction of Prostate Cancer Risk: Role of Frequent Ejaculation-Associated Mechanisms.

Hassan M, Flanagan T, Eshaq A, Altamimi O, Altalag H, Alsharif M Cancers (Basel). 2025; 17(5).

PMID: 40075690 PMC: 11898507. DOI: 10.3390/cancers17050843.


Inhibition of Scavenger Receptor Class B Type 1 (SR-B1) Expression and Activity as a Potential Novel Target to Disrupt Cholesterol Availability in Castration-Resistant Prostate Cancer.

Pandey M, Cuddihy G, Gordon J, Cox M, Wasan K Pharmaceutics. 2021; 13(9).

PMID: 34575583 PMC: 8467449. DOI: 10.3390/pharmaceutics13091509.


Androgen receptor isoforms expression in benign prostatic hyperplasia and primary prostate cancer.

Hillebrand A, Pizzolato L, Silva Neto B, Branchini G, Simoni Brum I PLoS One. 2018; 13(7):e0200613.

PMID: 30028845 PMC: 6054396. DOI: 10.1371/journal.pone.0200613.


Deletion of tumor suppressors adenomatous polyposis coli and Smad4 in murine luminal epithelial cells causes invasive prostate cancer and loss of androgen receptor expression.

Valkenburg K, De Marzo A, Williams B Oncotarget. 2017; 8(46):80265-80277.

PMID: 29113300 PMC: 5655195. DOI: 10.18632/oncotarget.17919.


Targeting AR Variant-Coactivator Interactions to Exploit Prostate Cancer Vulnerabilities.

Magani F, Peacock S, Rice M, Martinez M, Greene A, Magani P Mol Cancer Res. 2017; 15(11):1469-1480.

PMID: 28811363 PMC: 5770277. DOI: 10.1158/1541-7786.MCR-17-0280.


References
1.
GROSSMANN M, Huang H, Tindall D . Androgen receptor signaling in androgen-refractory prostate cancer. J Natl Cancer Inst. 2001; 93(22):1687-97. DOI: 10.1093/jnci/93.22.1687. View

2.
Stanbrough M, Bubley G, Ross K, Golub T, Rubin M, Penning T . Increased expression of genes converting adrenal androgens to testosterone in androgen-independent prostate cancer. Cancer Res. 2006; 66(5):2815-25. DOI: 10.1158/0008-5472.CAN-05-4000. View

3.
Titus M, Schell M, Lih F, Tomer K, Mohler J . Testosterone and dihydrotestosterone tissue levels in recurrent prostate cancer. Clin Cancer Res. 2005; 11(13):4653-7. DOI: 10.1158/1078-0432.CCR-05-0525. View

4.
Wu F, Mo Y . Ubiquitin-like protein modifications in prostate and breast cancer. Front Biosci. 2006; 12:700-11. DOI: 10.2741/2094. View

5.
Wilson J . The role of 5alpha-reduction in steroid hormone physiology. Reprod Fertil Dev. 2002; 13(7-8):673-8. DOI: 10.1071/rd01074. View