• 대한한방부인과학회지
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• 제22권4호
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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.

• 대한한방부인과학회지
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• 제22권3호
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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.

• Biomolecules & Therapeutics
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• 제30권5호
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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.

• Biomolecules & Therapeutics
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• 제11권2호
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• pp.151-156
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• 2003

Cornis fructus have various biological effects and major chemical components have been tannins, saponins, ursolic acids, gallic acids, linoleic acids, morronisides, cornins and loganins. The main aim of the present study is measurment the effect of chloroform extract from Cornis fructus on proliferation inhibition and Cell death. Cells were cultured in the presence of chloroform extracts from Cornis fructus for 48 h. after 48h treatment of B16/F10 melanoma cells with chloroform extracts, the cells were observed a dose-dependent inhibitions of cell viability with cell death in their proliferation. the cells were estimated cell viability, cell number, total DNA fragmentation and chromatin condensation in a dose-dependent manner. It also caused cell death as measured by cell morphology, DNA fragmentation and nucleus chromatin condensation. therefore, these results suggest that chloroform extracts from C. fructus is inhibitory proliferation and is related to cell death in this cells.

• 약학회지
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• 제46권1호
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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.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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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)

• 대한한방부인과학회지
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• 제22권4호
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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.

• 한국응용과학기술학회지
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• 제34권2호
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• pp.296-304
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• 2017

구아바 잎 추출물이 미백 기능성 화장품 소재로써의 활용 가능성을 확인하고자 하였다. DPPH radical 소거 활성, 세포 내 ROS 측정, B16F10 melanoma cell 에서의 세포 독성 및 자외선A에 대한 세포 보호효과, 시험관 내 tyrosinase 억제 효과, 멜라닌 생합성 억제 효과를 측정하였다. 구아바 잎 추출물의 높은 DPPH radical 소거 활성과, 세포 내 ROS 활성 억제 측정을 통해 항산화 효과를 확인하였다. B16F10 melanoma cell에서의 세포 생존율이 모든 농도에서 98% 이상의 생존율을 나타냈으며, UVA로부터의 세포 보호효과가 농도 의존적으로 높아지는 것을 확인하였다. 또한 10%의 시험관 내 tyrosinase 활성 억제 효과와 20%의 멜라닌 생합성 억제 효과를 확인되었다. 구아바 잎 추출물은 B16F10 melanoma cell에 대한 독성이 적고, 높은 항산화 활성과 tyrosinase 활성 억제 및 멜라닌 생합성 억제 효과를 통해 안전하고 우수한 미백 효과를 가진 미백 기능성 화장품 소재로써의 개발 가능성을 확인하였다.

• Journal of Microbiology and Biotechnology
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• 제25권12호
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• pp.1997-2006
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• 2015

Ginsenoside Rg3 is a bioactive ginseng constituent that has been reported to have diverse pathological and physiological effects, including anti-inflammatory and anti-metastatic activities. Metastasis is one of the most important factors involved in patients with melanoma. However, the molecular mechanism underlying the anti-metastatic activities of Rg3 in malignant melanoma cancer has not been fully elucidated. In this study, we have evaluated that Rg3 effectively inhibits metastasis of B16F10 melanoma cancer cells. We found that Rg3 significantly suppresses the migration, invasion, wound healing, and colony-forming abilities of B16F10 cells in a dose-dependent manner. Mechanistically, we demonstrate that Rg3 suppresses B16F10 cell metastasis by inhibiting MMP-13 expression. These results indicate that Rg3 suppresses the metastasis of B16F10 mouse melanoma cancer cells via MMP-13 regulation. Importantly, MMP-13 downregulation may influence the migration and invasion capabilities of melanoma cells and has been correlated with melanoma progression. Therefore, Rg3 is a potential therapeutic candidate that could be used to treat patients with metastatic melanoma.

• 대한의생명과학회지
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• 제29권3호
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• pp.201-205
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• 2023

Free adenine is mainly made during the polyamine synthesis in proliferating cells. Adenine molecule itself acts biological modulator in inflammation and cell death. In the previous report, we showed that adenine induces apoptotic cell death of B16-F10 mouse melanoma cells by eliciting of PARP and caspase 3 cleavages. In this study, we examined the adenine effect on other apoptotic molecules affecting caspase activation in B16-F10 melanoma cells. Adenine treatment make pro-apoptotic molecules active states. Bax/Bcl-2 ratio was increased and phosphorylation of mTOR and Akt was decreased in a dose dependent manner. These results showed the possibility that Bax/Bcl-2, Akt and mTOR are engaged in adenine induced apoptosis of melanoma cells.