Faculty Collaboration Database

2-arachidonoylglycerol: a novel inhibitor of androgen-independent prostate cancer cell invasion. Cancer Res 2004 Dec 15;64(24):8826-30

Date

12/18/2004

Pubmed ID

15604240

DOI

10.1158/0008-5472.CAN-04-3136

Scopus ID

2-s2.0-10844265493 (requires institutional sign-in at Scopus site)   122 Citations

Abstract

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.

Author List

Nithipatikom K, Endsley MP, Isbell MA, Falck JR, Iwamoto Y, Hillard CJ, Campbell WB

Authors

William B. Campbell PhD Professor in the Pharmacology and Toxicology department at Medical College of Wisconsin
Cecilia J. Hillard PhD Associate Dean, Center Director, Professor in the Pharmacology and Toxicology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Androgens
Arachidonic Acids
Cell Line, Tumor
Cyclic AMP-Dependent Protein Kinases
Cyclohexanones
Endocannabinoids
Glycerides
Humans
Hydrolysis
Lipoprotein Lipase
Male
Neoplasm Invasiveness
Neoplasms, Hormone-Dependent
Prostatic Neoplasms
Receptor, Cannabinoid, CB1