Butein induces G2/M phase arrest and apoptosis in human hepatoma cancer cells through ROS generation

被引：123

作者：

Moon, Dong-Oh ^{[1
]}

Kim, Mun-Ock ^{[1
]}

Choi, Yung Hyun ^{[2
]}

Hyun, Jin Won ^{[1
,3
]}

Chang, Weon Young ^{[1
,3
]}

Kim, Gi-Young ^{[1
]}

机构：

[1] Cheju Natl Univ, Dept Marine Life Sci, Immunobiol Lab, Cheju 690756, South Korea

[2] Dong Eui Univ, Coll Oriental Med, Dept Biochem, Pusan 614054, South Korea

[3] Cheju Natl Univ, Sch Med, Cheju 690756, South Korea

来源：

CANCER LETTERS | 2010年 / 288卷 / 02期

关键词：

Butein; G(2)/M phase arrest; Apoptosis; ROS; JNK; NF-KAPPA-B; HEPATOCELLULAR-CARCINOMA; MITOCHONDRIAL PATHWAY; DEPENDENT PATHWAY; PLANT POLYPHENOL; HL-60; CELLS; DNA-DAMAGE; ACTIVATION; PROLIFERATION; GROWTH;

D O I：

10.1016/j.canlet.2009.07.002

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We investigated the molecular effects of 3,4,2',4'-tetrahydroxychalcone (butein) treatment in two human hepatoma cancer cell lines-HepG2 and Hep3B. Butein treatment inhibited cancer cell growth by inducing G(2)/M phase arrest and apoptosis. Butein-induced G(2)/M phase arrest was associated with increased ATM, Chk1, and Chk2 phosphorylations and reduced cdc25C levels. Additionally, butein treatment enhanced inactivated phospho-Cdc2 levels, reduced Cdc2 kinase activity, and generated reactive oxygen species (ROS) that was accompanied by JNK activation. The extent of butein-induced G(2)/M phase arrest significantly decreased following pretreatment with N-acetyl-L-cysteine or glutathione and following JNK phosphorylation reduction by SP600125. Both N-acetyl-L-cysteine and glutathione also decreased butein-mediated apoptosis. Taken together, these results imply a critical role of ROS and JNK in the anticancer effects of butein. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

引用

页码：204 / 213

页数：10

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