Antaroide, a Novel Natural Nine-Membered Macrolide, Inhibits Melanin Biosynthesis in B16F10 Murine Melanoma Cells

Argan (Argania spinosaL.) oil has been used for centuries in Morocco as cosmetic oil to maintain a fair complexion and to cure skin pimples and chicken pox pustules scars. Although it is popular, the scientific basis for its effect on the skin has not yet been established. Here, the melanogenesis regulatory effect of argan oil was evaluated using B16 murine melanoma cells. Results of melanin assay using B16 cells treated with different concentrations of argan oil showed a dose-dependent decrease in melanin content. Western blot results showed that the expression levels of tyrosinase (TYR), tyrosinase-related protein 1 (TRP1), and dopachrome tautomerase (DCT) proteins were decreased. In addition, there was an increase in the activation of MITF and ERK1/2. Real-time PCR results revealed a downregulation ofTyr,Trp1,Dct, andMitfmRNA expressions. Argan oil treatment causes MITF phosphorylation which subsequently inhibited the transcription of melanogenic enzymes, TYR and DCT. The inhibitory effect of argan oil on melanin biosynthesis may be attributed to tocopherols as well as the synergistic effect of its components. The results of this study provide the scientific basis for the traditionally established benefits of argan oil and present its therapeutic potential against hyperpigmentation disorders.

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Thioredoxin Reductase Induction Coincides with Melanin Biosynthesis in Brown and Black Guinea Pigs and in Murine Melanoma Cells

Journal of Investigative Dermatology ◽

10.1111/1523-1747.ep12413557 ◽

1994 ◽

Vol 103 (6) ◽

pp. 820-824 ◽

Cited By ~ 20

Author(s):

Karin U Schallreuter ◽

K Regina Lemke ◽

Helene Z Hill ◽

John M Wood

Keyword(s):

Guinea Pigs ◽

Thioredoxin Reductase ◽

Melanoma Cells ◽

Melanin Biosynthesis ◽

Murine Melanoma ◽

Murine Melanoma Cells

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Antimelanogenic Effect of Purpurogallin in Murine Melanoma Cells

Journal of the Korean Society of Food Science and Nutrition ◽

10.3746/jkfn.2015.44.12.1905 ◽

2015 ◽

Vol 44 (12) ◽

pp. 1905-1911

Author(s):

Han-Hyuk Kim ◽

Tae Hoon Kim

Keyword(s):

Melanoma Cells ◽

Murine Melanoma ◽

Murine Melanoma Cells

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Anthocyanin determination in blueberry extracts from various cultivars and their antiproliferative and apoptotic properties in B16-F10 metastatic murine melanoma cells

Phytochemistry ◽

10.1016/j.phytochem.2013.06.018 ◽

2013 ◽

Vol 95 ◽

pp. 436-444 ◽

Cited By ~ 80

Author(s):

Andrea Bunea ◽

Dumitriţa Rugină ◽

Zoriţa Sconţa ◽

Raluca M. Pop ◽

Adela Pintea ◽

...

Keyword(s):

Melanoma Cells ◽

Murine Melanoma ◽

Murine Melanoma Cells

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Opposite effects of TPA on G1/S transition and on cell size in the low metastatic B16F1 with respect to high metastatic BL6 murine melanoma cells

Cancer Letters ◽

10.1016/s0304-3835(98)00177-3 ◽

1998 ◽

Vol 132 (1-2) ◽

pp. 159-164 ◽

Cited By ~ 4

Author(s):

Caterina A.M La Porta ◽

Danilo Porro ◽

Roberto Comolli

Keyword(s):

Cell Size ◽

Melanoma Cells ◽

Murine Melanoma ◽

Murine Melanoma Cells

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Regulation of c-met expression in B16 murine melanoma cells by melanocyte stimulating hormone

Journal of Cell Science ◽

10.1242/jcs.112.5.623 ◽

1999 ◽

Vol 112 (5) ◽

pp. 623-630

Author(s):

D. Rusciano ◽

P. Lorenzoni ◽

M.M. Burger

Keyword(s):

Melanoma Cells ◽

Parental Cell ◽

Melanocortin Receptor ◽

Parental Cell Line ◽

Melanocyte Stimulating Hormone ◽

Murine Melanoma ◽

The One ◽

Murine Melanoma Cells ◽

Stimulating Hormone

B16 murine melanoma cells selected in vivo for enhanced liver metastatic ability (B16-LS9) show on the one hand an increased expression and constitutive activation of the proto-oncogene c-met (the receptor for hepatocyte growth factor/scatter factor), and on the other hand a more differentiated phenotype, when compared to the parental cell line, B16-F1. Following this observation, we have tried to establish whether there is a direct relationship between differentiation and c-met expression in B16 melanoma cells. Treatment of these cells with differentiating agents indicated that c-met expression was strongly induced by melanocyte stimulating hormone, while retinoic acid had almost no influence. c-met induction was triggered by engagement of the melanocortin receptor, cAMP elevation and PKA/PKC(α) activation, as respectively shown by the effects of ACTH, cAMP elevating agents and specific PK inhibitors. Regulation of c-met expression via the melanocortin receptor and cAMP raises the intriguing possibility that autocrine and/or paracrine mechanisms acting in vivo on this circuit might influence (through c-met expression and activation) the metastatic behavior of these tumor cells, which we have shown to be dependent on their c-met expression.

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