Arachidonyl Ethanolamide Induces Apoptosis Of Uterine Cervix Cancer Cells

[Julie Gardener]

Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells
via aberrantly expressed vanilloid receptor-​

Emmanuel Contassot, Mirna Tenan, Valerie Schnuriger, Marie-Francoise Pelte, and Pierre-Yves Dietric
Gynecologic Oncology 93 (2004)

Abstract

-Tetrahydrocannabinol, the active agent of Cannabis sativa, exhibits well-documented antitumor properties, but little isknown about the possible effects mediated by endogenous cannabinoids on human tumors. In the present study, we analyzed the effect ofarachidonyl ethanolamide (AEA) on cervical carcinoma (CxCa) cell lines.

Methods: To assess the sensitivity of CxCa cells to AEA, we selected three cell lines that were exposed to increasing doses of AEA with or without antagonists to receptors to AEA. DNA fragmentation and caspase-7 activity were used as apoptosis markers. The expression of receptors to AEA were analyzed in CxCa cell lines as well as CxCa biopsies.

Results: The major finding was that AEA induced apoptosis of CxCa cell lines via aberrantly expressed vanilloid receptor-1, whereas AEA binding to the classical CB1 and CB2 cannabinoid receptors mediated a protective effect. Furthermore, unexpectedly, a strong expression of the three forms of AEA receptors was observed in ex vivo CxCa biopsies.

Conclusion: Overall, these data suggest that the specific targeting of VR1 by endogenous cannabinoids or synthetic molecules offers attractive opportunities for the development of novel potent anticancer drugs.

Source with Charts and Graphs: Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells
via aberrantly expressed vanilloid receptor-1