| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2019832 | Prostaglandins & Other Lipid Mediators | 2011 | 10 Pages |
Abstract
ⶠEndocannabinoids, protected from hydrolysis, inhibited prostate carcinoma cell proliferation. ⶠEndocannabinoids inhibited cell proliferation via the activation of cannabinoid type-1 receptor. ⶠNoladin ether, a putative and enzymatically stable endocannabinoid inhibited cell proliferation. ⶠThe proliferation inhibition by noladin ether was cannabinoid receptor- and PPARγ-independent. ⶠWater-soluble analogs of noladin ether may be practical and effective drugs for carcinoma cells.
Keywords
NF-κB2-oleoylglycerolDAKmGlFAAH2-arachidonoylglycerol2-AGPPARγCBRAEA2-OGendocannabinoidArachidonic acidFatty acid amide hydrolaseendocannabinoidsProliferationtumor necrosis factor-alphaProstate cancerTNF-αNuclear factor-kappa Bmonoacylglycerol lipasePeroxisome proliferator-activated receptor gammacannabinoid receptor
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Authors
Kasem Nithipatikom, Marilyn A. Isbell, Michael P. Endsley, Jeffrey E. Woodliff, William B. Campbell,