• The Journal of Korean Obstetrics and Gynecology
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• v.22 no.4
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• pp.1-18
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• 2009

Purpose: This study was performed to elucidate the inhibitory effect of Mibaeksan (MB) on melanin synthesis in B16F10 mouse melanoma cell. Methods: To demonstrate the inhibitory effects of MB on melanin synthesis, we measured the amount of released and produced melanin in B16F10 melanoma cell. Also, we evaluated tyrosinase-activity in vitro as well as in B16F10 melanoma cell. And to investigate the action mechanism, we assessed the gene expression of tyrosinase, TRP-1, TRP-2, MMP-2, PKA, $PKC{\beta}$, ERK-1 ERK-2, AKT-1 and MITF in B16F10 melanoma cells. Results: 1. MB decreased the release and production of melanin in B16F10 melanoma cells. 2. MB decreased tyrosinase activity in vitro and in B16F10 melanoma cells. 3. MB decreased the expression of tyrosinase, TRP-1, TRP-2, PKA, $PKC{\beta}$ and MMP-2 in B16F10 melanoma cells. 4. MB increased the expression of ERK-1, ERK-2 and AKT-1 in B16F10 melanoma cells. 5. MB decreased the expression of MITF in B16F10 melanoma cells. Conclusion: From these results, it may be concluded that MB has the antimelanogenetic effects.

• Biomolecules & Therapeutics
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• v.30 no.5
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• pp.465-472
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• 2022

Melanoma is one of the most aggressive skin cancers. Hypoxia contributes to the aggressiveness of melanoma by promoting cancer growth and metastasis. Upregulation of cyclin D1 can promote uncontrolled cell proliferation in melanoma, whereas stimulation of cytotoxic T cell activity can inhibit it. Epithelial mesenchymal transition (EMT) plays a critical role in melanoma metastasis. Hypoxia-inducible factor-1α (HIF-1α) is a main transcriptional mediator that regulates many genes related to hypoxia. CoCl₂ is one of the most commonly used hypoxia-mimetic chemicals in cell culture. In this study, inhibitory effects of IDF-11774, an inhibitor of HIF-1α, on melanoma growth and metastasis were examined using cultured B16F10 mouse melanoma cells and nude mice transplanted with B16F10 melanoma cells in the presence or absence of CoCl₂-induced hypoxia. IDF-11774 reduced HIF-1α upregulation and cell survival, but increased cytotoxicity of cultured melanoma cells under CoCl₂-induced hypoxia. IDF-11774 also reduced tumor size and local invasion of B16F10 melanoma in nude mice along with HIF-1α downregulation. Expression levels of cyclin D1 in melanoma were increased by CoCl₂ but decreased by IDF-11774. Apoptosis of melanoma cells and infiltration of cytotoxic T cells were increased in melanoma after treatment with IDF-11774. EMT was stimulated by CoCl₂, but restored by IDF11774. Overall, IDF-11774 inhibited the growth and metastasis of B16F10 melanoma via HIF-1α downregulation. The growth of B16F10 melanoma was inhibited by cyclin D1 downregulation and cytotoxic T cell stimulation. Metastasis of B16F10 melanoma was inhibited by EMT suppression.

• The Journal of Korean Obstetrics and Gynecology
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• v.22 no.3
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• pp.66-82
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• 2009

Purpose: This study was performed to elucidate the inhibitory effect of Yukmijihwangtang-gagambang (YMG) on melanin synthesis in B16F10 mouse melanoma cell. Methods: To demonstrate the inhibitory effects of YMG on melanin synthesis, we measured the amount of released and produced melanin in B16F10 melanoma cell. Also, we evaluated tyrosinase-activity in vitro as well as in B16F10 melanoma cell. And to investigate the action mechanism we assessed the gene expressions of tyrosinase, TRP-1, TRP-2, MMP-2, PKA, PKC${\beta}$, ERK-1 ERK-2, AKT-1 and MITF in B16F10 melanoma cells. Results: 1. YMG decreased the release and production of melanin in B16F10 melanoma cells. 2. YMG decreased tyrosinase activity in vitro and in B16F10 melanoma cells. 3. YMG decreased the expression of tyrosinase, TRP-1, TRP-2, PKA, PKC${\beta}$ and MMP-2 in B16F10 melanoma cells. 4. YMG increased the expression of ERK-1, ERK-2, and AKT-1 in B16F10 melanoma cells. 5. YMG decreased the expression of MITF in B16F10 melanoma cells. Conclusion: From these results, we suggest that YMG inhibit melanin synthesis via tyrosinase inhibition and regulation of the gene expression in B16F10 melanoma cells.

• The Journal of Korean Obstetrics and Gynecology
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• v.22 no.4
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• pp.28-45
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• 2009

Purpose: This study was performed to elucidate the inhibitory effect of Yukmijihwangtanghapyijihwangagambang (YM) on melanin synthesis in B16F10 melanoma cells. Methods: To demonstrate the inhibitory effects of YM on melanin synthesis, we measured the amount of released and produced melanin in B16F10 melanoma call. Also, we evaluated tyrosinase-activity in vitro as well as in B16F10 melanoma call. And to investigate the action mechanism, we assessed the gene expression of tyrosinase, TRP-1, TRP-2, PKA, $PKC{\beta}$, ERK-1 ERK-2, AKT-1 and MITF in B16F10 melanoma call. Results: 1. YM decreased the release and production of melanin in B16F10 melanoma cells. 2. YM decreased tyrosinase activity in vitro and in B16F10 melanoma cells. 3. YM decreased the expression of tyrosinase, TRP-1, TRP-2 in B16F10 melanoma cells. 4. YM decreased the expression of PKA, $PKC{\beta}$ in B16F10 melanoma cells. 5. YM increased the expression of ERK-1, ERK-2 and AKT-1 in B16F10 melanoma cells. 6. YM decreased the expression of MITF in B16F10 melanoma cells. Conclusion: From these results, it may be concluded that YM has antimelanogenetic effects.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.210.1-210.1
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• 2003

In this study, we investigated the effect of inhibition of proliferation and antioxidant effect on B16F10 murine melanoma cell. Also, we examined by MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and intracellular reactive oxygen intermediate levels and the levels of catalase(CAT), superoxide dismutase (SOD), and glutathione peroxidase(GPX) an adaptive response of oxidative stress on B16F10 murine melanoma cell of pretreated with hydrogen peroxide. (omitted)

• YAKHAK HOEJI
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• v.46 no.1
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• pp.75-80
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• 2002

Quercetin is one of the bioflavonoid compounds and has multiple biological effects such as antioxidant and effective anti-inflammatory agent. Melanin has an important role in protecting human skin from the damaging effects of ultra-violet W) radiation. We studied the effect of quercetin on proliferation of B16/F10 melanoma cells. After 48h treatment of cells with quercetin, the cells exhibited a dose-dependent inhibition in their proliferation without apoptosis. Therefore, the decrease in cell numbers may be due to cell growth arrest, not due to cell death by cytotoxicity. We also investigated the effect of quercetin on melanogenesis of this cells. B16/F10 melanoma cells were grown for 48h in the presence of 0.01~50$\mu\textrm{g}$/ml quercetin and the total melanin contents were measured. Quercetin stimulated melanization of the cells in low concentrations (0.01~20$\mu\textrm{g}$/ml), whereas it inhibited melanization in high concentrations (30~50$\mu\textrm{g}$/ml). It was observed that quercetin differently regulates melanogenesis of B16/F10 melanoma cells dependent on its concentrations.

• Journal of Life Science
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• v.23 no.12
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• pp.1516-1524
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• 2013

To find a novel skin whitening agent, the effect of cordycepin-enriched Cordyceps militaris (CM${\alpha}$) extract fermented by fungi on anti-melanogenesis in B16F0 mouse melanoma cells was investigated. Fermented CM${\alpha}$ was prepared with fungi, including Monascus purpureus (Mp), Aspergillus oryzae (Ao), Aspergillus kawachii (Ak), and Rhizopus oryzae (Ro), respectively. When the content of the phenolics and the flavonoids and the activities of the antioxidant and the mushroom tyrosinase inhibition were measured in the CM fermented by Ak (AkF-CM), the highest content of the phenolics was 46 mg/g dry weight and the highest content of the flavonoids was 0.93 mg/g; the highest activity of the DPPH radical scavenging was 62.74% and the highest activity of the mushroom tyrosinase inhibition was 79.97% CM${\alpha}$CM${\alpha}$. From this result, AkF-CM${\alpha}$ exhibited the highest mushroom tyrosinase inhibitory activity and so it was used in subsequent anti-melanogenesis. B16F0 melanoma cells were treated with 1-10 mg/ml concentrations of AkF-CM${\alpha}$ and 200 ${\mu}M$ arbutin as the positive control. The melanin content and cell viability of the melanoma cells by arbutin treatment decreased to 43% and 92% of the control, respectively. AkF-CM${\alpha}$ treatment at 1, 3, and 5 mg/ml concentrations decreased the extracellular melanin release induced by IBMX treatment by 35%, 45%, and 53%, respectively. AkF-CM${\alpha}$ showed inhibitory activity against both intracellular tyrosinase in melanoma cells and mushroom tyrosinase. AkF-CM${\alpha}$ reduced the protein level of tyrosinase in the IBMX-stimulated cells. These results indicate that AkF-CM${\alpha}$ suppressed the activity and protein content of cellular tyrosinase and decreased the total melanin content in cultured B16F0 melanoma cells.

• The Journal of Korean Obstetrics and Gynecology
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• v.22 no.1
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• pp.95-109
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• 2009

Purpose: This study was performed to determine the inhibitory effect of Sihosogansangagambang (SS) on melanin synthesis in B16F10 melanoma cells (B16F10). Methods: The inhibitory effects of Sihosogansangagambang on melanin synthesis were used by in vitro assay. To elucidate inhibitory effects of SS on melanin synthesis, we determined the melanin release in B16F10. And to investigate the mechanism of inhibitory effect of SS, we assessed the gene expression of tyrosinase, TRP-1, TRP-2 and ERK-1 in B16F10. Results: 1. SS decreased the release of melanin in B16F10 melanoma cells. 2. SS inhibited mushroom tyrosinase activity in vitro. 3. SS decreased the expression of tyrosinase, TRP-2 in B16F10 melanoma cells, but did not decreased the expression of TRP-1 in B16F10 melanoma cells. 4. SS decreased the expression of ERK-1 in B16F10 melanoma cells. Conclusion: From these results, it may be suggested that SS is possesed of the antimelanogenetic effects.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.3795-3802
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• 2012

Cochinchina momordica seeds (CMS) have been widely used due to antitumor activity by Mongolian tribes of China. However, the details of the underlying mechanisms remain unknown. In the present study, we found that an EtOAc (ethyl ester) extract of CMS (CMSEE) induced differentiation and caused growth inhibition of melanoma B16 F1 cells. CMSEE at the concentration of $5-200{\mu}g/ml$ exhibited strongest anti-proliferative effects on B16 F1 cells among other CMS fractions (water or petroleum ether). Moreover, CMSEE induced melanoma B16 F1 cell differentiation, characterized by dendrite-like outgrowth, increasing melanogenesis production, as well as enhancing tyrosinase activity. Western blot analysis showed that sustained phosphorylation of p38 MAP accompanied by decrease in ERK1/2 and JNK dephosphorylation were involved in CMSEE-induced B16 F1 cell differentiation. Notably, 6 compounds that were isolated and identified may be responsible for inducing differentiation of CMSEE. These results indicated that CMSEE contributes to the differentiation of B16 F1 cells through modulating MAPKs activity, which may throw some light on the development of potentially therapeutic strategies for melanoma treatment.

• YAKHAK HOEJI
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• v.56 no.4
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• pp.254-259
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• 2012

To further access honeybee (Apis mellifera L.) venom (BV) as a cosmetic ingredient and potential external treatment for topical use, we investigated its ability to inhibit tyrosinase activity and melanin biosynthesis on melanogenesis in B16F1 melanoma cells. We found that BV increased the cell viability in B16F1 melanoma cell and BV (0.01~1 ${\mu}g/ml$) inhibited melanin synthesis in with 10 nM ${\alpha}$-melanocyte-stimulating hormone (${\alpha}$-MSH) for 48 h. In addition, we used reverse transcription-polymerase chain reaction and western blotting for me melanogenesis-related genes such as tyrosinase to examine the mechanisms underlying the inhibitory effects of BV on melanogensis. BV inhibited direct tyrosinase activity, which decreased melanin synthesis in ${\alpha}$-MSH stimulated B16F1 melanoma cells. Thease findings suggest that BV induces the downregulation of melanogenesis by inhibiting tyrosinase activation.