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Involvement of Transglutaminase-2 in α-MSH-Induced Melanogenesis in SK-MEL-2 Human Melanoma Cellsopen access

Authors
Kim, Hyun JiLee, Hye JaPark, Mi KyungGang, Kyung JinByun, Hyun JungPark, Jeong HoKim, Mi KyungKim, Soo YoulLee, Chang Hoon
Issue Date
May-2014
Publisher
한국응용약물학회
Keywords
Cystamine; Melanogenesis; Transglutaminase-2; TRP-1; TRP-2; SK-MEL-2 melanoma cells
Citation
Biomolecules & Therapeutics , v.22, no.3, pp 207 - 212
Pages
6
Indexed
SCIE
SCOPUS
KCI
Journal Title
Biomolecules & Therapeutics
Volume
22
Number
3
Start Page
207
End Page
212
URI
https://scholarworks.dongguk.edu/handle/sw.dongguk/18230
DOI
10.4062/biomolther.2014.031
ISSN
1976-9148
2005-4483
Abstract
Skin hyperpigmentation is one of the most common skin disorders caused by abnormal melanogenesis. The mechanism and key factors at play are not fully understood. Previous reports have indicated that cystamine (CTM) inhibits melanin synthesis, though its molecular mechanism in melanogenesis remains unclear. In the present study, we investigated the effect of CTM on melanin production using ELISA reader and the expression of proteins involved in melanogenesis by Western blotting, and examined the involvement of transglutaminase-2 (Tgase-2) in SK-MEL-2 human melanoma cells by gene silencing. In the results, CTM dose-dependently suppressed melanin production and dendrite extension in alpha-MSH-induced melanogenesis of SK-MEL-2 human melanoma cells. CTM also suppressed alpha-MSH-induced chemotactic migration as well as the expressions of melanogenesis factors TRP-1, TRP-2 and MITF in alpha-MSH-treated SK-MEL-2 cells. Meanwhile, gene silencing of Tgase-2 suppressed dendrite extension and the expressions of TRP-1 and TRP-2 in alpha-MSH-treated SK-MEL-2 cells. Overall, these findings suggested that CTM suppresses alpha-MSH-induced melanogenesis via Tgase-2 inhibition and that therefore, Tgase-2 might be a new target in hyperpigmentation disorder therapy.
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