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

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• 作者：Yu-Wei  ; Chou^a ; Nagendra K.  ; Chaturvedi^a ; Shougiang  ; Ouyang^a ; Fen-Fen  ; Lin^a ; Dharam  ; Kaushik^a ;   ; ^b ; Jue  ; Wang^c ;   ; ^d ; Isaac  ; Kim^e ; Ming-Fong  ; Lin^a ;   ; ^d ;   ; ^{mlin@unmc.edu}
• 关键词：Prostate cancer ; HDAC inhibitors ; CPAcP ; ErbB-2 ; Androgen responsiveness
• 刊名：Cancer Letters
• 出版年：2011
• 出版时间：8 December 2011
• 年：2011
• 卷：311
• 期：2
• 页码：177-186
• 全文大小：903 K

文摘

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.