Etoposide induces growth arrest and disrupts androgen receptor signaling in prostate cancer cells

  • Authors:
    • Shicheng Liu
    • Hitoshi Yamauchi
  • View Affiliations

  • Published online on: January 1, 2010     https://doi.org/10.3892/or_00000618
  • Pages: 165-170
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Abstract

Androgen and androgen receptor (AR)-mediated signaling are crucial for the development of prostate cancer. The present study indicates that the topoisomerase II inhibitor etoposide strikingly inhibits androgen/AR-mediated cell growth and androgen-stimulated DNA synthesis in prostate cancer cells. Etoposide significantly repressed the AR mRNA and protein expression in a dose-dependent manner. Etoposide-mediated down-regulation of AR was associated with blocking androgen-induced AR translocation from cytoplasm into nucleus of cells. Additionally, etoposide disrupted the association of AR and heat shock protein 90 and impeded binding of the synthetic androgen [3H]R1881 to AR in LNCaP cells. Etoposide simultaneously reduced the intracellular and secreted PSA levels, a marker for the progression of prostate cancer. These findings collectively reveal that etoposide not only serves as a traditional genotoxic agent but directly targets AR as an AR disrupting therapeutic strategy in prostate cancer.

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January 2010
Volume 23 Issue 1

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Spandidos Publications style
Liu S and Yamauchi H: Etoposide induces growth arrest and disrupts androgen receptor signaling in prostate cancer cells. Oncol Rep 23: 165-170, 2010.
APA
Liu, S., & Yamauchi, H. (2010). Etoposide induces growth arrest and disrupts androgen receptor signaling in prostate cancer cells. Oncology Reports, 23, 165-170. https://doi.org/10.3892/or_00000618
MLA
Liu, S., Yamauchi, H."Etoposide induces growth arrest and disrupts androgen receptor signaling in prostate cancer cells". Oncology Reports 23.1 (2010): 165-170.
Chicago
Liu, S., Yamauchi, H."Etoposide induces growth arrest and disrupts androgen receptor signaling in prostate cancer cells". Oncology Reports 23, no. 1 (2010): 165-170. https://doi.org/10.3892/or_00000618