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Updated: Aug 6, 2026

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel
Published on: September 8, 2017
ACTR/AIB1/SRC-3 and androgen receptor control prostate cancer cell proliferation and tumor growth through direct
June X Zou1, Zhenyu Zhong, Xu-Bao Shi
1UC Davis Cancer Center/Basic Sciences, Department of Biochemistry & Molecular Medicine, University of California at Davis, School of Medicine, Sacramento, California, USA. jxzou@ucdavis.edu
Background:
Co-factor ACTR is frequently overexpressed and/or amplified in multiple types of tumors. The mechanism of its function in prostate cancer (CaP) is still unclear.
Methods:
The effects of ACTR and androgen receptor (AR) depletion on cell proliferation and gene expression and their functions were analyzed in a panel of androgen-dependent and -independent CaP cells and CWR22 xenograft.
Results:
ACTR and AR, but not TIF2, are required for proliferation of androgen-dependent and -independent cells, and for tumor growth. While AR depletion inhibited the expression of cyclin D1, cyclin B, and cdc2, ACTR depletion reduced the expression of cyclin E and cdk2. In response to serum stimulation, AR and ACTR are recruited to the corresponding target gene promoters to activate their expression in androgen-independent manner.
Conclusion:
These findings suggest that AR and ACTR may play important roles in androgen ablation resistance by controlling key cell cycle gene expression.
Insights
Androgen receptor (AR) and ACTR co-factor are crucial for prostate cancer cell growth and tumor development. They may drive resistance to androgen ablation therapy by regulating cell cycle genes.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Co-factor ACTR is frequently overexpressed and amplified in various tumors.
- The precise role of ACTR in prostate cancer (CaP) remains largely unknown.
Purpose of the Study:
- To investigate the functional role of ACTR and androgen receptor (AR) in prostate cancer progression.
- To elucidate the mechanism by which ACTR and AR influence cell proliferation and gene expression in CaP.
Main Methods:
- Analysis of ACTR and AR depletion effects on cell proliferation and gene expression.
- Utilized a panel of androgen-dependent and -independent CaP cell lines.
- Employed CWR22 xenograft models for in vivo studies.
Main Results:
- ACTR and AR are essential for the proliferation of both androgen-dependent and -independent CaP cells, as well as tumor growth.
- AR depletion affected expression of cyclins D1, B, and cdc2, while ACTR depletion impacted cyclin E and cdk2.
- Both AR and ACTR are recruited to target gene promoters for activation in an androgen-independent manner.
Conclusions:
- AR and ACTR play significant roles in prostate cancer.
- These co-factors may contribute to androgen ablation resistance.
- Their involvement in controlling key cell cycle gene expression is critical for CaP progression.
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