Concise Review: Androgen Receptor Differential Roles in Stem/Progenitor Cells Including Prostate, Embryonic, Stromal, and Hematopoietic Lineages

Authors

  • Chiung-Kuei Huang,

    1. Departments of Pathology, Urology, Radiation Oncology, the George Whipple Lab for Cancer Research, and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York, USA
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  • Jie Luo,

    1. Departments of Pathology, Urology, Radiation Oncology, the George Whipple Lab for Cancer Research, and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York, USA
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  • Soo Ok Lee,

    1. Departments of Pathology, Urology, Radiation Oncology, the George Whipple Lab for Cancer Research, and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York, USA
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  • Chawnshang Chang

    Corresponding author
    1. Departments of Pathology, Urology, Radiation Oncology, the George Whipple Lab for Cancer Research, and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York, USA
    2. Sex Hormone Research Center, China Medical University/Hospital, Taichung, Taiwan
    • Correspondence: Chang, Ph.D., George Whipple Lab for Cancer Research, University of Rochester Medical Center, Rochester, New York 14642. Telephone: 585-273-4500; Fax; 585-756-4133; e-mail: chang@urmc.rochester.edu

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Abstract

Stem/progenitor (S/P) cells are special types of cells that have the ability to generate tissues throughout their entire lifetime and play key roles in the developmental process. Androgen and the androgen receptor (AR) signals are the critical determinants in male gender development, suggesting that androgen and AR signals might modulate the behavior of S/P cells. In this review, we summarize the AR effects on the behavior of S/P cells, including self-renewal, proliferation, apoptosis, and differentiation in normal S/P cells, as well as proliferation, invasion, and self-renewal in prostate cancer S/P cells. AR plays a protective role in the oxidative stress-induced apoptosis in embryonic stem cells. AR inhibits the self-renewal of embryonic stem cells, bone marrow stromal cells, and prostate S/P cells, but promotes their differentiation except for adipogenesis. However, AR promotes the proliferation of hematopoietic S/P cells and stimulates hematopoietic lineage differentiation. In prostate cancer S/P cells, AR suppresses their self-renewal, metastasis, and invasion. Together, AR differentially influences the characteristics of normal S/P cells and prostate cancer S/P cells, and targeting AR might improve S/P cell transplantation therapy, especially in embryonic stem cells and bone marrow stromal cells. Stem Cells 2014;32:2299–2308

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