Journal
ONCOTARGET
Volume 8, Issue 21, Pages 34971-34979Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.16496
Keywords
ADT; estrogen receptor beta; 8 beta-VE2; androgen receptor; therapy resistance
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Funding
- Deutsche Forschungsgemeinschaft [TH 389/3-1, BU 992/6-1, JA 398/11-1, BR 4700/1-1]
- Open Access Publication Funds of Goettingen University
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Advanced prostate cancer can develop into castration-resistant prostate cancer (CRPC). This process is mediated either by intratumoral ligand synthesis or by mutations or aberrations of the androgen receptor (AR) or its cofactors. To date, no curative therapy for CRPC is available, as AR-targeted therapies eventually result in the development of resistance. The human prostate cancer cell line VCaP (vertebral cancer of the prostate) overexpresses AR and its splice variants (ARVs) as a mechanism of resistance to androgen-deprivation therapy (ADT) of external and intratumoral origin. In the present study, we demonstrate that stimulating estrogen receptor beta activity with the specific agonist 8 beta-VE2 in VCaP cells in successive stages of ADT induced a time-and dose-dependent decrease in cell survival and an increase in apoptosis. Furthermore, 8 beta-VE2 treatment reduced the overexpression of the AR as well as ARVs in VCaP cells under maximum ADT. Our results indicate that decreased survival of the androgen-dependent CRPC cells employing apoptosis together with the regulative effect on AR expression could have beneficial effects over current AR-targeting therapies.
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