The Inhibitory Mechanism of N-(4-Hydroxyphenyl) Retinamide on Prostaglandin E2 Synthesis in Squamous Cell Carcinoma Cell Line.
- Author:
Eui Gee HWANG
1
;
Jung Hyun KIM
;
Sung Ho MOON
;
Seung Hwan KIM
;
Dong Hee HAN
;
Su Ok LEE
;
Byung Hwa KIM
Author Information
1. Chungdam Seoul ENT Clinic, Seoul, Korea. hw26305@hanmail.net
- Publication Type:Original Article
- Keywords:
N-(4-Hydroxyphenyl) retinamide;
Carcinoma;
Squamous cell;
Prostaglandin E2
- MeSH:
Carcinoma, Squamous Cell*;
Cell Line*;
Dinoprostone*;
Prostaglandin-Endoperoxide Synthases;
Retinoids;
RNA, Messenger
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2003;46(6):496-501
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: It is well known that Prostaglandin E2 (PGE2) is the most predominant prostaglandin in squamous cell carcinoma and that PGE2 synthesis is suppressed by retinoid. The purpose of this study was to confirm whether (N-4-Hydroxyphenyl) retinamide (N-4-HPR) suppressed PGE2 synthesis, and investigate its inhibitory mechanism on PGE2 synthesis in squamous cell carcinoma. MATERIALS AND METHOD: MDA 886Ln was used as the squamous cell carcinoma cell line. We evaluated the effects of four retinoids (all-trans-RA, 13-cis-RA, retinyl acetate, and N-4-HPR) on PGE2 synthesis: the effect of N-4-HPR concentration on PGE2 synthesis and Cox-2 mRNA, the effect of N-4-HPR on Cox-2 protein, and the effect of N-4-HPR on the cyclooxygenase activity. RESULTS: Among the four retinoids, N-4-HPR was the most potent suppressor of PGE2 synthesis. N-4-HPR suppressed PGE2 synthesis, but N-4-HPR did not suppress Cox-2 mRNA or Cox-2 protein. Cyclooxygenase activity was suppressed by N-4-HPR. CONCLUSION: With these results, we suggest that the inhibitory mechanism of N-4-HPR on the PGE2 synthesis may be suppression of the cyclooxygenase activity, and Cox-2 mRNA and protein were not suppressed by N-4-HPR.
