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Sphingosine 1-phosphate triggers apoptotic signal for 1316 melanoma cells via ERK and caspase activation

Title
Sphingosine 1-phosphate triggers apoptotic signal for 1316 melanoma cells via ERK and caspase activation
Authors
Shin, Jeong-HyunChoi, Gwang-SeongKang, Won-HytingMyung, Ki-Bum
Ewha Authors
명기범
SCOPUS Author ID
명기범scopusscopus
Issue Date
2007
Journal Title
JOURNAL OF KOREAN MEDICAL SCIENCE
ISSN
1011-8934JCR Link
Citation
vol. 22, no. 2, pp. 298 - 304
Keywords
sphingosine 1-phosphatemelanomaapoptosiscaspasesextracellular signal-regulated kinase
Publisher
KOREAN ACAD MEDICAL SCIENCES
Indexed
SCI; SCIE; SCOPUS; KCI WOS scopus
Abstract
The bioactive sphingolipid metabolite sphingosine 1-phosphate (S1P), recently was reported to induce apoptosis of some cancer cells and neurons, although it generally known to exert mitogenic and antiapoptotic effects. In this study, we investigated the effects of S1P on the cell growth, melanogenesis, and apoptosis of cultured B16 mouse melanoma cells. In results, S1P was found to induce apoptosis in B16 melanoma cells in a dose- and time-dependent manner, but exerted minimal effects on melanogenesis. Although receptors of sphingosine 1-phosphate (endothelial differentiation gene 1 [Edg]S1P1, Edg5/S1P2, Edg3/S1P3) were expressed in B16 melanoma cells, they were shown not to be associated with S1P-induced apoptosis. In addition, pertussis toxin did not block the apoptotic effects of S1P on B16 melanoma cells. S1P induced caspase-3 activation and the extracellular signal-regulated kinase (ERK) activation. Interestingly, the ERK pathway inhibitor, UO126, reversed the apoptotic effects of S1P on B16 melan ' oma cells. These results suggest that S1P induced apoptosis of B16 melanoma cells via an Edg receptor-independent, pertussis toxin-insensitive pathway, and appears to be associated with the ERK and caspase-3 activation.
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