Suppression of nerve growth factor Trk receptors and prolactin receptors by endocannabinoids leads to inhibition of human breast and prostate cancer cell proliferation.

摘要: Anandamide and 2-arachidonoylglycerol (2-AG), two endogenous ligands of the CB1 CB2 cannabinoid receptor subtypes, inhibit proliferation PRL-responsive human breast cancer cells (HBCCs) through down-regulation long form PRL (PRLr). Here we report that 1) anandamide 2-AG nerve growth factor (NGF)-induced HBCCs suppression levels NGF Trk receptors; 2) inhibition PRLr results in other cells, prostate DU-145 cell line; 3) CB1-like receptors are expressed mediate Trk/PRLr expression. β-NGF-induced HBCC was potently inhibited (IC50 = 50–600 nm) by synthetic HU-210, 2-AG, anandamide, its metabolically stable analogs, but not congener, palmitoylethanolamide, or selective agonist receptors, BML-190. Th...