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.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Nithipatikom K,Endsley MP,Isbell MA,Falck JR,Iwamoto Y,Hillard CJ,Campbell WBdoi
10.1158/0008-5472.CAN-04-3136subject
Has Abstractpub_date
2004-12-15 00:00:00pages
8826-30issue
24eissn
0008-5472issn
1538-7445pii
64/24/8826journal_volume
64pub_type
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