Licochalcone A inhibits growth of gastric cancer cells by arresting cell cycle progression and inducing apoptosis

被引:142
作者
Xiao, Xiu-ying [1 ,2 ,4 ]
Hao, Miao [3 ]
Yang, Xin-ying [3 ]
Ba, Qian [3 ]
Li, Mian [3 ]
Ni, Shu-juan [1 ,2 ]
Wang, Li-sha [1 ,2 ]
Du, Xiang [1 ,2 ]
机构
[1] Fudan Univ, Dept Pathol, Shanghai Canc Ctr, Shanghai 200032, Peoples R China
[2] Fudan Univ, Dept Oncol, Shanghai Med Coll, Shanghai 200032, Peoples R China
[3] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Nutr & Metab, Shanghai 200031, Peoples R China
[4] Shanghai Xuhui Dist Ctr Hosp, Dept Oncol, Shanghai 200031, Peoples R China
关键词
Licochalcone A; Gastric cancer; Cell viability; Apoptosis; Cell cycle; NF-KAPPA-B; CARCINOMA; LICORICE; PROLIFERATION; ACTIVATION; THERAPY; DRUGS; BCL-2;
D O I
10.1016/j.canlet.2010.12.016
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The aim of this study was to determine the anticancer effects of seven licorice compounds in MKN-28, AGS, and MKN-45 gastric cancer cells and human gastric epithelium immortalized cells. We also explored the mechanism of action of licochalcone A (LCA), the most cytotoxic licorice compound, by analyzing its influence on cell cycle progression and apoptosis. The results indicated that LCA was the most cytotoxic licorice compound of those tested, and it inhibited gastric cancer cells growth in a dose-dependent manner, with an IC50 value of approximately 40 mu M. LCA affected gastric cancer cell viability by blocking cell cycle progression at the G2/M transition and inducing apoptosis. LCA treatment increased the expression of Rb and decreased the expression of cyclin A, cyclin B and MDM2 in MKN-28, AGS and MKN-45 cell lines. In addition, LCA-induced apoptosis by its effects on the expression of PARP, caspase-3, Bcl-2 and Bax. These data provide evidence that LCA has the potential to be used in the treatment of gastric cancer. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:69 / 75
页数:7
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