Our natural cannabinoids fight melanoma

Our natural cannabinoids fight melanoma

September 18, 2013

This study found that anandamide, a cannabinoid created by our bodies, triggers changes in melanoma cancer cells that causes them to die. Anadamide causes cytotoxicity in melanoma cells. The plant cannabinoid THC from marijuana has activity that is very similar to anadamide and should be tested for use as a treatment for melanoma as soon as our pathetic political leaders change the laws that make research into marijuana’s benefits nearly impossible to conduct. J’accuse Barbara Boxer, Dianne Feinstein, Nancy Pelosi with crimes against humanity for their refusal to defend California’s medical marijuana laws. Using marijuana regularly lowers incidences of: cancer, diabetes, heart disease, age-related dementia and more. Don’t you owe it to your health to start using some form of marijuana? You don’t have to get high to stay well.
Eur J Pharmacol. 2013 Sep 13. pii: S0014-2999(13)00648-1. doi: 10.1016/j.ejphar.2013.08.039. [Epub ahead of print]
Anticancer activity of anandamide in human cutaneous melanoma cells.
Adinolfi B, Romanini A, Vanni A, Martinotti E, Chicca A, Fogli S, Nieri P.
Source
Department of Pharmacy, University of Pisa, Via Bonanno 6, Pisa, Italy.. Electronic address: badinolfi@yahoo.it.
Abstract
Cannabinoids are implicated in the control of cell proliferation, but little is known about the role of the endocannabinoid system in human malignant melanoma. This study was aimed at characterizing the in vitro antitumor activity of anandamide (AEA) in A375 melanoma cells. The mRNA expression of genes that code for proteins involved in the metabolism and in the mechanism of AEA action was assessed by RT-PCR. Cell viability was tested using WST-1 assay and the apoptotic cell death was determined by measuring caspase 3/7 activities. A375 cells express high levels of fatty acid amide hydrolase (FAAH), cyclooxygenase (COX)-2, cannabinoid receptor 1 (CB1), transient receptor potential cation channel subfamily V member 1 (TRPV1) and G-protein-coupled receptor 55 (GPR55) genes. AEA induced a concentration-dependent cytotoxicity with an IC50 of 5.8±0.7µM and such an effect was associated to a caspase-dependent apoptotic pathway. AEA cytotoxicity was potentiated by FAAH inhibition (2-fold increase, p<0 .05="" 3-fold="" a="" action.="" activation.="" activation="" aea.="" aea="" affected="" against="" agonist="" also="" and="" antagonism="" barely="" blocking="" by="" cb1="" cells="" cholesterol="" completely="" complex="" concentrations="" cox-2="" cyclodextrin="" cytotoxicity="" decrease="" decreased="" demonstrate="" depletory="" finally="" findings="" gpr55="" have="" human="" in="" induced="" induces="" inhibition="" involve="" linked="" lipid="" lipoxygenase="" lox-derived="" mechanism="" melanoma="" membrane="" methyl-="" micromolar="" might="" mitigated="" modulation="" o-1602="" of="" on="" or="" overall="" p="" partially="" probably="" product="" raft="" range="" receptors="" respectively="" reversed="" role.="" selective="" span="" synthesis="" that="" the="" these="" through="" to="" trpv1="" whereas="" which="">
Copyright © 2013. Published by Elsevier B.V.
via Anticancer activity of anandamide in human c… [Eur J Pharmacol. 2013] – PubMed – NCBI.