Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 332, Issue 4, Pages 1028-1033Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2005.05.049
Keywords
2-arachidonoylglycerol; cell invasion; endocannabinoid; carboxylesterase inhibitors; prostate cancer
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Funding
- NIDA NIH HHS [R01 DA009155, DA 09155] Funding Source: Medline
- NIDDK NIH HHS [T32 DK007355, T32 DK07355-22] Funding Source: Medline
- NIEHS NIH HHS [P42 ES004699, P30 ES005707, P42 ES04699, R37 ES02710, R37 ES002710, P30 ES05707] Funding Source: Medline
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Endogenous 2-arachidonoylglycerol (2-AG) inhibits invasion of androgen-independent prostate cancer cells. Blocking cellular hydrolysis of 2-AG to increase its endogenous concentration results in a decrease in cell invasion. A series of compounds containing a trifluoromethyl ketone (TFK) moiety or the methyl analog (known to inhibit carboxylesterases) were investigated for their ability to inhibit 2-AG hydrolysis and prostate cancer cell invasion. Compounds containing a thioether P to a TFK moiety inhibited 2-AG hydrolysis as well as cell invasion in a concentration-dependent manner. Inhibition of 2-AG hydrolysis increased concomitantly with inhibitor alkyl chain length from 4- to 12-carbons while inhibition of cell invasion exhibited a maximum at 8- to 10-carbons of the compounds. These results demonstrate a new series of 2-AG hydrolysis inhibitors as a potential therapeutic approach for prostate cancer. (c) 2005 Elsevier Inc. All rights reserved.
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