1-monooleoyl-rac-glycerol and 1-6-bis(cyclohexyloximinocarbonyl)hexane

1-monooleoyl-rac-glycerol has been researched along with 1-6-bis(cyclohexyloximinocarbonyl)hexane* in 1 studies

Other Studies

1 other study(ies) available for 1-monooleoyl-rac-glycerol and 1-6-bis(cyclohexyloximinocarbonyl)hexane

Article	Year
2-arachidonoylglycerol: a novel inhibitor of androgen-independent prostate cancer cell invasion. Cancer research, 2004, Dec-15, Volume: 64, Issue:24 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. Topics: 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	2004

Article

Year

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

Cancer research, 2004, Dec-15, Volume: 64, Issue:24

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.

Topics: 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

2004