4.6 Article

EGCG suppresses prostate cancer cell growth modulating acetylation of androgen receptor by anti-histone acetyltransferase activity

Journal

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
Volume 30, Issue 1, Pages 69-74

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2012.966

Keywords

epigallocatechin-3-gallate; histone acetyltransferase; prostate cancer; androgen receptor; acetylation

Funding

  1. Ministry of Health & Welfare, Republic of Korea [A100011]
  2. Korea Health Promotion Institute [A100011] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Manipulating acetylation status of key gene targets is likely to be crucial for effective cancer therapy. In this study, we utilized green tea catechins, epicatechin (EC), epigallocatechin (EGC) and epigallocatechin-3-gallate (EGCG) to examine the regulation of androgen receptor acetylation in androgen-dependent prostate cancer cells by histone acetyltransferase (HAT) activity. EC, EGC and EGCG induced prostate cancer cell death, suppressed agonist-dependent androgen receptor (AR) activation and AR-regulated gene transcription. These results demonstrated a similar tendency to HAT inhibitory activities; EGCG>EGC>EC. The strongest HAT inhibitor among them, EGCG (50 mu M), downregulated AR acetylation and finally, AR protein translocation to nucleus from the cytoplasmic compartment was effectively inhibited in the presence of the agonist. These results suggest another mechanism to develop effective therapeutics based on green tea catechins.

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