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Anandamide inhibits proliferation of oral squamous cell carcinoma
Author(s) -
Flynn Andrea N,
Schmidt Brian L
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.729.16
Subject(s) - endocannabinoid system , anandamide , fatty acid amide hydrolase , trpv1 , monoacylglycerol lipase , cannabinoid receptor , cell growth , pharmacology , chemistry , cannabinoid , cancer research , medicine , biochemistry , receptor , antagonist , transient receptor potential channel
Cancer patients experience severe, unmanageable pain. Patients often develop tolerance and suffer side effects from opioids. The endocannabinoid system includes the cannabinoid receptors (CBr1, CBr2), the endogenous ligands, anandamide (AEA) and 2‐ arachidonoylglycerol (2‐AG), and their cognate degradative enzymes, fatty acid amide hydrolase and monoacylglycerol lipase (MAGL). Endocannabinoids have recently emerged as potential antitumor agents. However, their effect on head and neck cancer remains undefined. We monitored the proliferation of an oral carcinoma cell line, HSC3, over 24 hours using the xCELLigence Real‐Time Cell Analyzer. We found AEA inhibited proliferation with an IC 50 of 1.05 μM. We also found Ki67, a marker of proliferation, was significantly reduced following addition of 5 μM AEA for 24 hours. HSC3 proliferation was also reduced following treatment with PF‐750, an irreversible inhibitor of FAAH. AEA has been shown to activate CBr1, CBr2, and TRPV1. Preliminary experiments with specific inhibitors to CBr1, CBr2, and TRPV1 indicate AEA elicits these anti‐proliferative effects via CBr1 and TRPV1. These results indicate regulation of the endocannabinoid system could be a promising treatment for oral cancer and associated pain.