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Anticancer effects of anandamide on head and neck squamous cell carcinoma cells via the production of receptor‐independent reactive oxygen species
Author(s) -
Park SeokWoo,
Kim JiEun,
Oh SangMi,
Cha WonJae,
Hah JeongHun,
Sung MyungWhun
Publication year - 2015
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.23727
Subject(s) - anandamide , head and neck squamous cell carcinoma , fatty acid amide hydrolase , endocannabinoid system , chemistry , cannabinoid receptor , reactive oxygen species , cell growth , receptor , intracellular , cell culture , cancer research , squamous carcinoma , cell , pharmacology , medicine , biology , biochemistry , cancer , carcinoma , antagonist , head and neck cancer , genetics
Background The endocannabinoids, anandamide (AEA) and 2‐arachidonoyl glycerol (2‐AG), are considered promising potential anticancer agents. In this study, we examined the anticancer effects of AEA and 2‐AG in head and neck squamous cell carcinoma (HNSCC) cell lines. Methods and Results Our results showed that AEA effectively inhibited proliferation of HNSCC cells whereas 2‐AG did not. The anticancer effect of AEA seemed to be mediated by a receptor‐independent mechanism. Inhibitors of AEA intracellular transportation and transfection of HNSCC cells with fatty acid amide hydrolase, a key enzyme in AEA metabolism, reversed AEA‐dependent inhibition of cell proliferation. We found that cyclooxygenase‐2 (COX‐2) did not mediate the anticancer effects of AEA; instead we observed an increase in reactive oxygen species (ROS) production after AEA treatment. Moreover, antioxidants partially reversed AEA‐dependent inhibition of cell proliferation. Conclusion These findings suggest that AEA might have anticancer effects on HNSCC cells by mediating an increase in ROS levels through a receptor‐independent mechanism. © 2014 Wiley Periodicals, Inc. Head Neck 37: 1187–1192, 2015