title: EGCG suppresses prostate cancer cell growth modulating acetylation of             androgen receptor by anti-histone acetyltransferase activity.
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 acetyl-transferase (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.
authors.affiliation: Department of Food Science and Nutrition, The University of Suwon,                     Kyunggi-do, Republic of Korea.
authors.forename: Yoo-Hyun
authors.initials: YH
authors.lastname: Lee
authors.forename: Jieun
authors.initials: J
authors.lastname: Kwak
authors.forename: Hyo-Kyoung
authors.initials: HK
authors.lastname: Choi
authors.forename: Kyung-Chul
authors.initials: KC
authors.lastname: Choi
authors.forename: Sunoh
authors.initials: S
authors.lastname: Kim
authors.forename: Jeongmin
authors.initials: J
authors.lastname: Lee
authors.forename: Woojin
authors.initials: W
authors.lastname: Jun
authors.forename: Hyun-Jin
authors.initials: HJ
authors.lastname: Park
authors.forename: Ho-Geun
authors.initials: HG
authors.lastname: Yoon
mesh_terms: D000107:Acetylation / Q000187:drug effects; D059002:Androgen Receptor Antagonists / Q000494:pharmacology*; D000970:Antineoplastic Agents / Q000378:metabolism / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D002392:Catechin / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D018890:Chemoprevention; D051548:Histone Acetyltransferases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D006801:Humans; D008297:Male; D011471:Prostatic Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000517:prevention & control; D011944:Receptors, Androgen / Q000378:metabolism*; D014158:Transcription, Genetic / Q000187:drug effects
chemical_list: D059002:Androgen Receptor Antagonists; D000970:Antineoplastic Agents; D011944:Receptors, Androgen; D002392:Catechin; C045651:epigallocatechin gallate; D051548:Histone Acetyltransferases; C057580:gallocatechol