Are androgen receptor variants a substitute for the full-length receptor?
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Updated: Apr 17, 2026

Detecting the Ligand-binding Domain Dimerization Activity of Estrogen Receptor Alpha Using the Mammalian Two-Hybrid Assay
Published on: December 19, 2018
Ji Lu1, Travis Van der Steen2, Donald J Tindall3
1Department of Urology, First Hospital of Jilin University, 71 Xinmin Street, Changchun 130021, China.
Abstract:
Androgen receptor splice variants (AR-Vs)--which are expressed in castration-resistant prostate cancer (CRPC) cell lines and clinical samples--lack the C-terminal ligand-binding domain and are constitutively active. AR-Vs are, therefore, resistant to traditional androgen deprivation therapy (ADT). AR-Vs are induced by several mechanisms, including ADT, and might contribute to the progression of CRPC and resistance to ADT. AR-Vs could represent a novel therapeutic target for prostate cancer, especially in CRPC.
Insights
Androgen receptor splice variants (AR-Vs) are active in prostate cancer and resist treatment. Targeting AR-Vs may offer a new therapeutic strategy for castration-resistant prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Urology
Background:
- Androgen receptor splice variants (AR-Vs) are present in castration-resistant prostate cancer (CRPC).
- AR-Vs lack the ligand-binding domain, leading to constitutive activity.
- These variants are resistant to conventional androgen deprivation therapy (ADT).
Purpose of the Study:
- To investigate the role of AR-Vs in CRPC.
- To explore AR-Vs as a potential therapeutic target.
Main Methods:
- Analysis of AR-V expression in CRPC cell lines and clinical samples.
- Characterization of AR-V activity and resistance mechanisms.
Main Results:
- AR-Vs are expressed in CRPC.
- Constitutive activity of AR-Vs contributes to ADT resistance.
- AR-V induction can be triggered by ADT.
Conclusions:
- AR-Vs are key drivers in CRPC progression and treatment resistance.
- Targeting AR-Vs presents a promising therapeutic avenue for advanced prostate cancer.
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