http://www.cnr.it/ontology/cnr/individuo/prodotto/ID196928

Cannabimimetic fatty acid derivatives in cancer and inflammation (Articolo in rivista)

Type

Prodotto della ricerca (Classe)
Articolo in rivista (Classe)

Label

Cannabimimetic fatty acid derivatives in cancer and inflammation (Articolo in rivista) (literal)

Anno

2000-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.1016/S0090-6980(00)00054-X (literal)

Alternative label

Di Marzo V, Melck D, De Petrocellis L, Bisogno T. (2000)
Cannabimimetic fatty acid derivatives in cancer and inflammation
in Prostaglandins & other lipid mediators (Print); Elsevier Science Inc., New York (Stati Uniti d'America)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Di Marzo V, Melck D, De Petrocellis L, Bisogno T. (literal)

Pagina inizio

43 (literal)

Pagina fine

61 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

61 (literal)

Rivista

Prostaglandins & other lipid mediators (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

1-2 (literal)

Note

ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

1. CNR, Ist Chim Mol Interesse Biol, I-80072 Arco, Napoli, Italy 2. CNR, Ist Cibernetica, I-80072 Arco, Italy 3. CNR, Inst Chem Biol Syst, I-00185 Rome, Italy (literal)

Titolo

Cannabimimetic fatty acid derivatives in cancer and inflammation (literal)

Abstract

Evidence for the role of the cannabimimetic fatty acid derivatives (CFADs), i.e. anandamide (arachidonoylethanolamide, AEA), 2-arachidonoylglycerol (2-AG) and palmitoylethanolamide (PEA), in the control of inflammation and of the proliferation of tumor cells is reviewed here. The biosynthesis of AEA, PEA, or 2-AG can be induced by stimulation with either Ca2+ ionophores, lipopolysaccharide, or platelet activating factor in macrophages, and by ionomycin or antigen challenge in rat basophilic leukemia (RBL-2H3) cells (a widely used model for mast cells). These cells also inactivate CFADs through re-uptake and/or hydrolysis and/or esterification processes. AEA and PEA modulate cytokine and/or arachidonate release from macrophages in vitro, regulate serotonin secretion from RBL-2H3 cells, and are analgesic in some animal models of inflammatory pain. However, the involvement of endogenous CFADs and cannabinoid CB1 and CB2 receptors in these effects is still controversial. In human breast and prostate cancer cells, AEA and 2-AG, but not PEA, potently inhibit prolactin and/or nerve growth factor (NGF)-induced cell proliferation. Vanillyl-derivatives of anandamide, such as olvanil and arvanil, exhibit even higher anti-proliferative activity. These effects are due to suppression of the levels of the 100 kDa prolactin receptor or of the high affinity NGF receptors (trk), are mediated by CB1-like cannabinoid receptors, and are enhanced by other CFADs. Inhibition of adenylyl cyclase and activation of mitogen-activated protein kinase underlie the anti-mitogenic actions of AEA. The possibility that CFADs act as local inhibitors of the proliferation of human breast cancer is discussed here. (literal)

Editore