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

Lee,Yoo-Hyun; Kwak,Jieun; Choi,Hyo-Kyoung; Choi,Kyung-Chul; Kim,Sunoh; Lee,Jeongmin; Jun,Woojin; Park,Hyun-Jin; Yoon,Ho-Geun

doi:10.3892/ijmm.2012.966

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

Authors:
- Yoo-Hyun Lee
- Jieun Kwak
- Hyo-Kyoung Choi
- Kyung-Chul Choi
- Sunoh Kim
- Jeongmin Lee
- Woojin Jun
- Hyun-Jin Park
- Ho-Geun Yoon
View Affiliations

Affiliations: Department of Food Science and Nutrition, The University of Suwon, Kyunggi-do, Republic of Korea, Brain Korea 21 Life Science and Biotechnology, Korea University, Seoul, Republic of Korea, Department of Biochemistry and Molecular Biology, Center for Chronic Metabolic Disease Research, College of Medicine, Yonsei University, Seoul, Republic of Korea, Department of Medicine, Graduate School, University of Medicine, Seoul, Republic of Korea, Jeollanamdo Institute of Natural Resources Research, Jeonnam, Republic of Korea, Department of Medical Nutrition, Kyung Hee University, Kyunggi-do, Republic of Korea, Department of Food and Nutrition, Chonnam National University, Gwangju, Republic of Korea
Published online on: April 10, 2012 https://doi.org/10.3892/ijmm.2012.966
Pages: 69-74

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

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 µM), 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.