[6]-Gingerol Suppresses Colon Cancer Growth by Targeting Leukotriene A4 Hydrolase

被引：148

作者：

Jeong, Chul-Ho ^{[1
]}

Bode, Ann M. ^{[1
]}

Pugliese, Angelo ^{[1
]}

Cho, Yong-Yeon ^{[1
]}

Kim, Hong-Gyum ^{[1
]}

Shim, Jung-Hyun ^{[1
]}

Jeon, Young-Jin ^{[1
,2
]}

Li, Honglin ^{[3
,4
]}

Jiang, Hualiang ^{[3
,4
]}

Dong, Zigang ^{[1
]}

机构：

[1] Univ Minnesota, Hormel Inst, Austin, MN 55912 USA

[2] Chosun Univ, Coll Med, Dept Pharmacol, Gwanju, South Korea

[3] Chinese Acad Sci, Drug Discovery & Design Ctr, State Key Lab Drug Res, Shanghai Inst Mat Med, Beijing 100864, Peoples R China

[4] E China Univ Sci & Technol, Sch Pharm, Shanghai 200237, Peoples R China

来源：

CANCER RESEARCH | 2009年 / 69卷 / 13期

关键词：

NF-KAPPA-B; INFLAMMATORY RESPONSES; IN-VIVO; INHIBITORS; MICE; CHEMOPREVENTION; EXPRESSION; BESTATIN; DOCKING; ENZYME;

D O I：

10.1158/0008-5472.CAN-09-0491

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

[6]-Gingerol, a natural component of ginger, exhibits anti-inflammatory and antitumorigenic activities. Despite its potential efficacy in cancer, the mechanism by which [6]-gingerol exerts its chemopreventive effects remains elusive. The leukotriene A(4) hydrolase (LTA(4)H) protein is regarded as a relevant target for cancer therapy. Our in silico prediction using a reverse-docking approach revealed that LTA(4)H might be a potential target of [6]-gingerol. We supported our prediction by showing that [6]-gingerol suppresses anchorage-independent cancer cell growth by inhibiting LTA(4)H activity in HCT116 colorectal cancer cells. We showed that [6]-gingerol effectively suppressed tumor growth in vivo in nude mice, an effect that was mediated by inhibition of LTA(4)H activity. Collectively, these findings indicate a crucial role of LTA(4)H in cancer and also support the anticancer efficacy of [6]-gingerol targeting of LTA(4)H for the prevention of colorectal cancer. [Cancer Res 2009;69(13):5584-91]

引用

页码：5584 / 5591

页数：8

共 35 条

[1]

Gingerol metabolite and a synthetic analogue Capsarol™ inhibit macrophage NF-κB-mediated iNOS gene expression and enzyme activity [J].