Antitumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma
J Pharmacol Exp Ther. 2006-05-25; 318(3): 1375-1387
DOI: 10.1124/jpet.106.105247
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1. J Pharmacol Exp Ther. 2006 Sep;318(3):1375-87. doi: 10.1124/jpet.106.105247.
Epub 2006 May 25.
Antitumor activity of plant cannabinoids with emphasis on the effect of
cannabidiol on human breast carcinoma.
Ligresti A(1), Moriello AS, Starowicz K, Matias I, Pisanti S, De Petrocellis L,
Laezza C, Portella G, Bifulco M, Di Marzo V.
Author information:
(1)Istituto di Chimica Biomolecolare, Consiglio Nazionale delle Ricerche
Pozzuoli, Italy.
Delta(9)-Tetrahydrocannabinol (THC) exhibits antitumor effects on various cancer
cell types, but its use in chemotherapy is limited by its psychotropic activity.
We investigated the antitumor activities of other plant cannabinoids, i.e.,
cannabidiol, cannabigerol, cannabichromene, cannabidiol acid and THC acid, and
assessed whether there is any advantage in using Cannabis extracts (enriched in
either cannabidiol or THC) over pure cannabinoids. Results obtained in a panel
of tumor cell lines clearly indicate that, of the five natural compounds tested,
cannabidiol is the most potent inhibitor of cancer cell growth (IC(50) between
6.0 and 10.6 microM), with significantly lower potency in noncancer cells. The
cannabidiol-rich extract was equipotent to cannabidiol, whereas cannabigerol and
cannabichromene followed in the rank of potency. Both cannabidiol and the
cannabidiol-rich extract inhibited the growth of xenograft tumors obtained by
s.c. injection into athymic mice of human MDA-MB-231 breast carcinoma or rat
v-K-ras-transformed thyroid epithelial cells and reduced lung metastases
deriving from intrapaw injection of MDA-MB-231 cells. Judging from several
experiments on its possible cellular and molecular mechanisms of action, we
propose that cannabidiol lacks a unique mode of action in the cell lines
investigated. At least for MDA-MB-231 cells, however, our experiments indicate
that cannabidiol effect is due to its capability of inducing apoptosis via:
direct or indirect activation of cannabinoid CB(2) and vanilloid transient
receptor potential vanilloid type-1 receptors and cannabinoid/vanilloid
receptor-independent elevation of intracellular Ca(2+) and reactive oxygen
species. Our data support the further testing of cannabidiol and
cannabidiol-rich extracts for the potential treatment of cancer.
DOI: 10.1124/jpet.106.105247
PMID: 16728591 [Indexed for MEDLINE]