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

June X. Zou, Zhenyu Zhong, Xu Bao Shi, Clifford G. Tepper, Ralph W. DeVere White, Hsing Jien Kung, Hongwu Chen

Research output: Contribution to journalArticle

32 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1474-1486
Number of pages13
JournalProstate
Volume66
Issue number14
DOIs
Publication statusPublished - Oct 1 2006
Externally publishedYes

Fingerprint

cdc Genes
Androgen Receptors
Prostatic Neoplasms
Androgens
Cell Proliferation
Growth
Neoplasms
Cyclin B
Gene Expression
Cyclin E
Cyclin D1
Heterografts
Serum
Genes

Keywords

  • Androgen independence
  • Androgen receptor
  • Cell cycle
  • Co-activators

ASJC Scopus subject areas

  • Oncology
  • Urology

Cite this

ACTR/AIBI/SRC-3 and androgen receptor control prostate cancer cell proliferation and tumor growth through direct control of cell cycle genes. / Zou, June X.; Zhong, Zhenyu; Shi, Xu Bao; Tepper, Clifford G.; DeVere White, Ralph W.; Kung, Hsing Jien; Chen, Hongwu.

In: Prostate, Vol. 66, No. 14, 01.10.2006, p. 1474-1486.

Research output: Contribution to journalArticle

Zou, June X. ; Zhong, Zhenyu ; Shi, Xu Bao ; Tepper, Clifford G. ; DeVere White, Ralph W. ; Kung, Hsing Jien ; Chen, Hongwu. / ACTR/AIBI/SRC-3 and androgen receptor control prostate cancer cell proliferation and tumor growth through direct control of cell cycle genes. In: Prostate. 2006 ; Vol. 66, No. 14. pp. 1474-1486.
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AU - Zhong, Zhenyu

AU - Shi, Xu Bao

AU - Tepper, Clifford G.

AU - DeVere White, Ralph W.

AU - Kung, Hsing Jien

AU - Chen, Hongwu

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N2 - 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.

AB - 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.

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KW - Cell cycle

KW - Co-activators

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