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.
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CITATION STYLE
Scherrmann, J.-M., Wolff, K., Franco, C. A., Potenza, M. N., Uzbay, T., Bizarro, L., … Leonard, B. E. (2010). 2-Arachidonoylglycerol. In Encyclopedia of Psychopharmacology (pp. 151–151). Springer Berlin Heidelberg. https://doi.org/10.1007/978-3-540-68706-1_537
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