Document Type


Journal Title

Cancer letters

Publication Date





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.

MeSH Headings

Antineoplastic Agents, Blotting, Northern, Blotting, Western, Cell Line, Tumor, Cell Proliferation, Cell Separation, Flow Cytometry, Histone Deacetylase Inhibitors, Humans, Male, Phosphorylation, Prostatic Neoplasms, Protein Tyrosine Phosphatases, Receptor, erbB-2, Valproic Acid




NOTICE: this is the author’s version of a work that was accepted for publication in Cancer Letters. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Cancer Letters, [VOL#311, ISSUE#2, (2011)] DOI#10.1016/j.canlet.2011.07.015