Histone deacetylase inhibitor valproic acid suppresses the growth and increases the androgen responsiveness of prostate cancer cells

Yu Wei Chou, Nagendra K. Chaturvedi, Shougiang Ouyang, Fen Fen Lin, Dharam Kaushik, Jue Wang, Isaac Kim, Ming-Fong Lin

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

We identified the molecular target by histone deacetylase (HDAC) inhibitors for exploring their potential prostate cancer (PCa) therapy. Upon HDAC inhibitors-treatment, LNCaP cell growth was suppressed, correlating with increased cellular prostatic acid phosphatase (cPAcP) expression, an authentic protein tyrosine phosphatase. In those cells, ErbB-2 was dephosphorylated, histone H3/H4 acetylation and methylation increased and cyclin proteins decreased. In PAcP shRNA-transfected C-81 cells, valproic acid (VPA) efficacy of growth suppression was diminished. Further, VPA pre-treatment enhanced androgen responsiveness of C-81, C4-2 and MDA PCa2b-AI cells. Thus, cPAcP expression is involved in growth suppression by HDAC inhibitors in PCa cells, and VPA pre-treatments increase androgen responsiveness.

Original languageEnglish (US)
Pages (from-to)177-186
Number of pages10
JournalCancer Letters
Volume311
Issue number2
DOIs
StatePublished - Dec 8 2011

Keywords

  • Androgen responsiveness
  • CPAcP
  • ErbB-2
  • HDAC inhibitors
  • Prostate cancer

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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