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Prostate. 2006 Oct 1;66(14):1474-86.

ACTR/AIB1/SRC-3 and androgen receptor control prostate cancer cell proliferation and tumor growth through direct control of cell cycle genes.

Author information

1
UC Davis Cancer Center/Basic Sciences, Department of Biochemistry & Molecular Medicine, University of California at Davis, School of Medicine, Sacramento, California, USA. jxzou@ucdavis.edu

Abstract

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.

PMID:
16921507
DOI:
10.1002/pros.20477
[Indexed for MEDLINE]

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