Journal
BMB REPORTS
Volume 45, Issue 12, Pages 724-729Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2012.45.12.039
Keywords
Caffeoylserotonin; Cyclic AMP; ERK; Melanogenesis; MITF
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Funding
- Korea Healthcare technology R&D Project, Ministry of Health Welfare [A103017]
- National Research Foundation of Korean Grant
- Korean Government [2011-0027021]
- Priority Research Centers Program through the National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2012-0005857]
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In this study, we evaluated the anti-melanogenesis effects of Caffeoylserotonin (CaS) in B16 melanoma cells. Treatment with CaS reduced the melanin content and tyrosinase (TYR) activity in B16 melanoma cells in a dose-dependent manner. CaS inhibited the expression of melanogenesis-related proteins, including microphthalmia-associated transcription factor (MITF), TYR, and tyrosinase-related protein-1 (TRP-1), but not TRP-2. alpha-MSH is known to interact with melanocortin 1 receptor (MC1R) thus activating adenylyl cyclase and increasing intracellular cyclic AMP (cAMP) levels. Furthermore, cAMP activates extracellular signal-regulated kinase 2 (ERK2) via phosphorylation, which phosphorylates MITE, thereby targeting the transcription factor to proteasomes for degradation. The CaS reduced intracellular cAMP levels to unstimulated levels and activated ERK phosphotylation within 30 min. The ERK inhibitor PD98059 abrogated the suppressive effect of CaS on alpha-MSH-induced melanogenesis. Based on this study, the inhibitory effects of CaS on melanogenesis are derived from the downregulation of MITF signaling via the inhibition of intracellular cAMP levels, as well as acceleration of ERK activation, [BMB Reports 2012; 45(12): 724-729]
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