A derivative of 2-aminothiazole inhibits melanogenesis in B16 mouse melanoma cells via glycogen synthase kinase 3β phosphorylation
- A derivative of 2-aminothiazole inhibits melanogenesis in B16 mouse melanoma cells via glycogen synthase kinase 3β phosphorylation
- 김수연; 한호규; 남기달; 박경찬; 윤혜영; 백광진; 권년수; 김동석
- tyrosinase; 2-aminothiazole; melanoma cell; GSK-3b; KHG25855; α-melanocyte stimulating hormone; glycogen synthase kinase 3β; melanogenesis
- Issue Date
- Journal of pharmacy and pharmacology
- VOL 63, NO 8, 1031-1036
- Objectives We have investigated whether KHG25855 (2-cyclohexylamino-1,3-thiazole
hydrochloride) affected melanogenesis in B16 mouse melanoma cells, and the mechanisms
Methods Melanin content and tyrosinase activity were measured using an ELISA reader
after cells were treated with KHG25855. KHG25855-induced signalling pathways were
examined using Western blot analysis.
Key findings KHG25855 decreased melanin production in a dose-dependent fashion, but
KHG25855 did not directly inhibit tyrosinase, the rate-limiting melanogenic enzyme. The
expression of microphthalmia-associated transcription factor, tyrosinase, and the related
signal transduction pathways were also investigated. The effects of KHG25855 on the
extracellular signal-regulated kinase and cAMP response element binding protein signalling
pathways were determined, and KHG25855 was shown to have no effect on these signalling
pathways. The Wnt signalling pathway is also deeply involved in melanogenesis, and so
glycogen synthase kinase 3β (GSK3β) phosphorylation was assessed after KHG25855
treatment; KHG25855 caused GSK3β phosphorylation (inactivation), but the level of
β-catenin was not changed by KHG25855. Furthermore, a-melanocyte stimulating
hormone-induced tyrosinase expression was downregulated by KHG25855.
Conclusions We propose that KHG25855 showed hypopigmentary activity through tyrosinase
downregulation via GSK3β phosphorylation.
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