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5-lipoxygenase mediates docosahexaenoyl ethanolamide and N-arachidonoyl-L-alanine-induced reactive oxygen species production and inhibition of proliferation of head and neck squamous cell carcinoma cells

DC Field Value Language
dc.contributor.authorPark, Seok-Woo-
dc.contributor.authorHah, J. Hun-
dc.contributor.authorOh, Sang-Mi-
dc.contributor.authorJeong, Woo-Jin-
dc.contributor.authorSung, Myung-Whun-
dc.date.accessioned2017-02-08T04:28:39Z-
dc.date.available2017-02-08T04:28:39Z-
dc.date.issued2016-07-13-
dc.identifier.citationBMC Cancer, 16(1):458ko_KR
dc.identifier.urihttps://hdl.handle.net/10371/100539-
dc.descriptionThis article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made.
ko_KR
dc.description.abstractAbstract

Background
Endocannabinoids have recently drawn attention as promising anti-cancer agents. We previously observed that anandamide (AEA), one of the representative endocannabinoids, effectively inhibited the proliferation of head and neck squamous cell carcinoma (HNSCC) cell lines in a receptor-independent manner. In this study, using HNSCC cell lines, we examined the anti-cancer effects and the mechanisms of action of docosahexaenoyl ethanolamide (DHEA) and N-arachidonoyl-L-alanine (NALA), which are polyunsaturated fatty acid (PUFA)-based ethanolamides like AEA.


Methods and Results
DHEA and NALA were found to effectively inhibit HNSCC cell proliferation. These anti-proliferative effects seemed to be mediated in a cannabinoid receptor-independent manner, since the antagonist of cannabinoid receptor-1 (CB1) and vanilloid receptor-1 (VR1), two endocannabinoid receptors, did not reverse the ability of DHEA and NALA to induce cell death. Instead, we observed an increase in reactive oxygen species (ROS) production and a decrease of phosphorylated Akt as a result of DHEA and NALA treatment. Antioxidants efficiently reversed the inhibition of cell proliferation and the decrease of phosphorylated Akt induced by DHEA and NALA; inhibition of 5-lipoxygenase (5-LO), which is expected to be involved in DHEA- and NALA-degradation pathway, also partially blocked the ability of DHEA and NALA to inhibit cell proliferation and phosphorylated Akt. Interestingly, ROS production as a result of DHEA and NALA treatment was decreased by inhibition of 5-LO.


Conclusions
From these findings, we suggest that ROS production induced by the 5-LO pathway mediates the anti-cancer effects of DHEA and NALA on HNSCC cells. Finally, our findings suggest the possibility of a new cancer-specific therapeutic strategy, which utilizes 5-LO activity rather than inhibiting it.
ko_KR
dc.language.isoenko_KR
dc.publisherBioMed Centralko_KR
dc.subjectEndocannabinoidko_KR
dc.subjectDHEAko_KR
dc.subjectNALAko_KR
dc.subject5-lipoxygenaseko_KR
dc.subjectROSko_KR
dc.subjectHead and neck cancerko_KR
dc.title5-lipoxygenase mediates docosahexaenoyl ethanolamide and N-arachidonoyl-L-alanine-induced reactive oxygen species production and inhibition of proliferation of head and neck squamous cell carcinoma cellsko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor박석우-
dc.contributor.AlternativeAuthor오상미-
dc.contributor.AlternativeAuthor정우진-
dc.contributor.AlternativeAuthor성명훈-
dc.identifier.doi10.1186/s12885-016-2499-3-
dc.language.rfc3066en-
dc.rights.holderThe Author(s).-
dc.date.updated2017-01-06T10:14:15Z-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Dept. of Medicine (의학과)Journal Papers (저널논문_의학과)
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