2-arachidonoylglycerol: A novel inhibitor of androgen-independent prostate cancer cell invasion

被引：111

作者：

Nithipatikom, K

Endsley, MP

Isbell, MA

Falck, JR

Iwamoto, Y

Hillard, CJ

Campbell, WB

机构：

[1] Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA

[2] Med Coll Wisconsin, Dept Urol, Milwaukee, WI 53226 USA

[3] Univ Texas, SW Med Ctr, Dept Biochem, Dallas, TX USA

[4] Univ Texas, SW Med Ctr, Dept Pharmacol, Dallas, TX USA

来源：

CANCER RESEARCH | 2004年 / 64卷 / 24期

关键词：

D O I：

10.1158/0008-5472.CAN-04-3136

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Endocannabinoids have been implicated in cancer. Increasing endogenous 2-arachidonoylglycerol (2-AG) by blocking its metabolism inhibits invasion of androgen-independent prostate cancer (PC-3 and DU-145) cells. Noladin ether (a stable 2-AG analog) and exogenous CB1 receptor agonists possess similar effects. Conversely, reducing endogenous 2-AG by inhibiting its synthesis or blocking its binding to CB1 receptors with antagonists increases the cell invasion. 2-AG and noladin ether decrease protein kinase A activity in these cells, indicating coupling of the CB1 receptor to downstream effectors. The results suggest that cellular 2-AG, acting through the CB1 receptor, is an endogenous inhibitor of invasive prostate cancer cells.

引用

页码：8826 / 8830

页数：5

共 20 条

[1] Brain monoglyceride lipase participating in endocannabinoid inactivation [J].