BACKGROUND AND OBJECTIVES: It is well known that Prostaglandin E(2) (PGE(2)) is the most predominant prostaglandin in squamous cell carcinoma and that PGE(2) synthesis is suppressed by retinoid. The purpose of this study was to confirm whether
N-(4-Hydroxyphenyl) retinamide (N-4-HPR) suppressed PGE(2) synthesis, and investigate its inhibitory mechanism on PGE(2) 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 PGE(2) synthesis : the effect of N-4-HPR concentration on PGE(2) 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 PGE(2) synthesis. N-4-HPR suppressed PGE(2) 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 PGE(2) synthesis may be suppression of the cyclooxygenase activity, and Cox-2 mRNA and protein were not suppressed by N-4-HPR.
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