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Updated: May 31, 2026

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
Published on: April 26, 2017
A new trick of an old molecule: androgen receptor splice variants taking the stage?!
1Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Abstract:
Prostate cancer is the second leading cause of cancer-related death in American men. Although most prostate cancers are initially androgen-dependent and respond to androgen ablation therapy, majority of them eventually relapse and progress into incurable castration-resistant (or hormone refractory) prostate cancer. The underlying mechanisms are the focus of intensive investigation for development of more effective treatment. Mounting evidence from both clinical and basic research has demonstrated that the activity of the androgen receptor (AR) is still required for castration-resistant prostate cancer. Multiple mechanisms by which AR is re-activated under androgen-depleted conditions may be involved in the development of castration resistance. The recent identification of AR splicing variants may add another layer of complexity in AR biology. The present review summarizes recent progress in study of AR splicing variants in prostate cancer.
Insights
Prostate cancer often becomes resistant to hormone therapy. This review explores androgen receptor (AR) splicing variants, which may explain how prostate cancer progresses to a more aggressive, incurable form.
Area of Science:
- Oncology
- Molecular Biology
- Urology
Background:
- Prostate cancer is a leading cause of cancer death in men.
- Most prostate cancers initially respond to androgen deprivation therapy.
- However, many progress to castration-resistant prostate cancer (CRPC).
Purpose of the Study:
- To review recent advancements in understanding androgen receptor (AR) biology in prostate cancer.
- To focus on the role of AR splicing variants in CRPC development.
Main Methods:
- Literature review of clinical and basic research studies.
- Analysis of current findings on AR signaling pathways.
- Examination of the impact of AR splicing variants.
Main Results:
- Androgen receptor (AR) activity remains crucial for CRPC progression.
- AR can be reactivated through various mechanisms under low-androgen conditions.
- AR splicing variants represent a significant factor in CRPC development.
Conclusions:
- Understanding AR reactivation mechanisms is key to developing new treatments.
- AR splicing variants add complexity to AR biology in prostate cancer.
- Further research into AR variants is essential for effective CRPC therapies.
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