Disruption of androgen receptor function inhibits proliferation of androgen-refractory prostate cancer cells

Ofelia L. Zegarra-Moro, Lucy J. Schmidt, Haojie Huang, Donald J. Tindall

Research output: Contribution to journalArticle

358 Scopus citations

Abstract

Prostate cancer cells depend on androgens and the androgen receptor (AR) for survival. However, after androgen ablation therapy, tumors relapse to an androgen-refractory state. To determine whether the androgen receptor is critical for proliferation of androgen-refractory prostate cancer cells, we disrupted the activity of the androgen receptor with an antibody and an AR mRNA hammerhead ribozyme in the following cell lines: LNCaP (androgen-sensitive), LNCaP-Rf and LNCaP-C4 (androgen-refractory), and DU-145 (androgen-insensitive). Microinjection of either antibody or ribozyme inhibited proliferation of androgen-refractory cells. These findings demonstrate that the AR is critical for proliferation of androgen-refractory cells, even in the absence of androgens.

Original languageEnglish (US)
Pages (from-to)1008-1013
Number of pages6
JournalCancer research
Volume62
Issue number4
StatePublished - 2002

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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