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Updated: Mar 14, 2026

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
Emerging data on androgen receptor splice variants in prostate cancer
Subing Cao1,2, Yang Zhan1,2, Yan Dong3,2
1College of Life SciencesJilin University, Changchun, Jilin, China.
Abstract:
Androgen receptor splice variants are alternatively spliced variants of androgen receptor, which are C-terminally truncated and lack the canonical ligand-binding domain. Accumulating evidence has indicated a significant role of androgen receptor splice variants in mediating resistance of castration-resistant prostate cancer to current therapies and in predicting therapeutic responses. As such, there is an urgent need to target androgen receptor splicing variants for more effective treatment of castration-resistant prostate cancer. Identification of precise and critical targeting points to deactivate androgen receptor splicing variants relies on a deep understanding of how they are generated and the mechanisms of their action. In this review, we will focus on the emerging data on their generation, clinical significance and mechanisms of action as well as the therapeutic influence of these findings.
Insights
Androgen receptor splice variants drive castration-resistant prostate cancer. Targeting these variants offers a promising therapeutic strategy for improving treatment outcomes in advanced prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Androgen receptor splice variants (AR-Vs) are truncated forms of the androgen receptor.
- AR-Vs play a crucial role in castration-resistant prostate cancer (CRPC) progression.
- AR-Vs are implicated in therapeutic resistance to current prostate cancer treatments.
Purpose of the Study:
- To review the generation mechanisms of AR-Vs.
- To elucidate the clinical significance and action mechanisms of AR-Vs.
- To discuss the therapeutic implications of targeting AR-Vs in CRPC.
Main Methods:
- Literature review of recent studies on AR-Vs.
- Analysis of data on AR-V generation and function.
- Synthesis of information on clinical relevance and therapeutic strategies.
Main Results:
- AR-Vs are generated through alternative splicing and lack the ligand-binding domain.
- AR-Vs are key mediators of resistance in CRPC.
- Understanding AR-V generation and action is critical for developing targeted therapies.
Conclusions:
- Targeting AR-Vs is essential for effective CRPC treatment.
- Further research into AR-V mechanisms will guide novel therapeutic approaches.
- AR-V targeted therapies hold promise for overcoming treatment resistance in prostate cancer.
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