trans-Resveratrol inhibits H2O2-induced adenocarcinoma gastric cells proliferation via inactivation of MEK1/2-ERK1/2-c-Jun signalling axis

被引：25

作者：

Aquilano, Katia ^{[1
]}

Baldelli, Sara ^{[1
]}

Rotilio, Giuseppe ^{[1
,2
]}

Ciriolo, Maria Rosa ^{[1
,2
]}

机构：

[1] Univ Roma Tor Vergata, Dept Biol, I-00133 Rome, Italy

[2] Res Ctr IRCCS San Raffaele, I-00165 Rome, Italy

来源：

BIOCHEMICAL PHARMACOLOGY | 2009年 / 77卷 / 03期

关键词：

Hydrogen peroxide; ERK1/2; Resveratrol; c-Jun; Cell proliferation; HYDROGEN-PEROXIDE; NITRIC-OXIDE; CANCER CHEMOPREVENTION; REGULATED KINASE; RECEPTOR; ANTIOXIDANTS; AGENT; GLUTATHIONE; SUPEROXIDE; METABOLISM;

D O I：

10.1016/j.bcp.2008.10.034

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

In this report we investigate the signalling pathway activated by H2O2 in human adenocarcinoma gastric cells (AGS) and we evaluate the anti-proliferative action of the natural stilbene trans-resveratrol. We demonstrate that H2O2 accelerates cell growth and induces a prompt MEK1/2-ERK1/2 activation. Such events are also associated with the activation of c-Jun and its translocation into the nuclear compartment. A specific inhibitor of ERK1/2 phosphorylation by MEK1/2 (U0126) abrogates these phenomena. On the contrary, specific inhibition of JNK activity does not influence H2O2-mediated growth, suggesting that cell proliferation likely proceeds via MEK1/2-ERK1/2-Jun signalling axis. trans-Resveratrol is also able to completely suppress the increase in proliferation. We demonstrate that this property is not due to its antioxidant capacity but rather due to a specific inhibition of ERK1/2 phosphorylation by MEK1/2 and repression of c-Jun activation. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：337 / 347

页数：11

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