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Updated: Apr 17, 2026

Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses
Published on: October 24, 2019
Cell-cycle-dependent regulation of androgen receptor function
Yulia Koryakina1, Karen E Knudsen1, Daniel Gioeli2
1Department of MicrobiologyImmunology, and Cancer Biology, University of Virginia, Jordan Hall Room 2-16, 1300 Jefferson Park Avenue, PO Box 800734, Charlottesville, Virginia 22908, USASidney Kimmel Cancer CenterThomas Jefferson University, Philadelphia, Pennsylvania, USACancer Center MemberUniversity of Virginia, Charlottesville, Virginia, USA.
Androgen receptor (AR) activity in prostate cancer is cell-cycle dependent. Mitotic phosphorylation of AR by CDK1 regulates its localization and transcriptional activity, impacting AR oncogene function.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- The androgen receptor (AR) is a key oncogene in prostate cancer (PCa) progression.
- AR activity, localization, and phosphorylation are crucial for PCa development.
Purpose of the Study:
- To investigate the cell-cycle-dependent regulation of AR activity, localization, and phosphorylation in prostate cancer.
- To elucidate the role of CDK1 in AR phosphorylation during mitosis.
Main Methods:
- Utilized imaging techniques, flow cytometry, and quantitative analysis.
- Employed phospho-S308 AR-specific antibodies and IP-western blotting.
- Performed in vitro kinase assays and pharmacological inhibition of CDK1.
Main Results:
- AR transactivation is highest in G1 phase and abrogated in G2/M phase.
- AR is excluded from chromatin during mitosis, correlating with S308 phosphorylation.
- CDK1 phosphorylates AR on S308 during mitosis, regulating its localization and activity.
Conclusions:
- Mitotic phosphorylation of AR by CDK1 is a critical regulatory mechanism.
- This phosphorylation impacts AR localization and transcriptional activity, influencing AR's role as an oncogene.
- Findings offer insights into AR function in prostate cancer progression.
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