Epigallocatechin-3-gallate up-regulates tumor suppressor gene expression via a reactive oxygen species-dependent down-regulation of UHRF1

被引：63
作者：
Achour, Mayada [1 ]
Mousli, Marc [1 ]
Alhosin, Mahmoud [1 ]
Ibrahim, Abdulkhaleg [1 ]
Peluso, Jean [2 ]
Muller, Christian D. [2 ]
Schini-Kerth, Valerie B. [1 ]
Hamiche, Ali [3 ]
Dhe-Paganon, Sirano [4 ,5 ]
Bronner, Christian [1 ]
机构：
[1] Univ Strasbourg, Fac Pharm, CNRS, UMR 7213,Lab Biophoton & Pharmacol, F-67401 Illkirch Graffenstaden, France
[2] Univ Strasbourg, Fac Pharm, CNRS, UMR 7200,Lab Innovat Therapeut, F-67401 Illkirch Graffenstaden, France
[3] Univ Strasbourg, CNRS, INSERM, Inst Genet & Biol Mol & Cellulaire, F-67401 Illkirch Graffenstaden, France
[4] Univ Toronto, Struct Genom Consortium, Toronto, ON M5G 1L7, Canada
[5] Univ Toronto, Dept Physiol, Toronto, ON M5G 1L7, Canada
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2013年 / 430卷 / 01期
关键词：
DNA methyltransferase 1; Epigallocatechin-3-gallate; P16(INK4A); Tumor suppressor gene; Ubiquitin-like containing PHD and Ring finger 1; II-ALPHA EXPRESSION; TRAIL-MEDIATED APOPTOSIS; CCAAT-BINDING-PROTEIN; HEMI-METHYLATED DNA; CANCER-CELLS; SRA DOMAIN; SKIN PHOTOPROTECTION; JURKAT CELLS; ICBP90; (-)-EPIGALLOCATECHIN-3-GALLATE;
D O I：
10.1016/j.bbrc.2012.11.087
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Ubiquitin-like containing PHD and Ring finger 1 (UHRF1) contributes to silencing of tumor suppressor genes by recruiting DNA methyltransferase I (DNMT1) to their hemi-methylated promoters. Conversely, demethylation of these promoters has been ascribed to the natural anti-cancer drug, epigallocatechin-3-gallate (EGCG). The aim of the present study was to investigate whether the UHRF1/DNMT1 pair is an important target of EGCG action. Here, we show that EGCG down-regulates UHRF1 and DNMT1 expression in Jurkat cells, with subsequent up-regulation of p73 and p16(INK4A) genes. The down-regulation of UHRF1 is dependent upon the generation of reactive oxygen species by EGCG. Up-regulation of p16(INK4A) is strongly correlated with decreased promoter binding by UHRF1. UHRF1 over-expression counteracted EGCG-induced G1-arrested cells, apoptosis, and up-regulation of p16(INK4A) and p73. Mutants of the Set and Ring Associated (SRA) domain of UHRF1 were unable to down-regulate p16(INK4A) and p73, either in the presence or absence of EGCG. Our results show that down-regulation of UHRF1 is upstream to many cellular events, including G1 cell arrest, up-regulation of tumor suppressor genes and apoptosis. (C) 2012 Elsevier Inc. All rights reserved.
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页码：208 / 212
页数：5
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