Suppression of α-MSH and IBMX-induced melanogenesis by cordycepin via inhibition of CREB and MITF, and activation of PI3K/Akt and ERK-dependent mechanisms

Jin, Mei Ling; Park, Sun Young; Kim, Young Hun; Park, Geuntae; Son, Hong-Joo; Lee, Sang-Joon

doi:10.3892/ijmm.2011.807

Cited by 18 publications

(13 citation statements)

References 23 publications

(24 reference statements)

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“…Melanogenesis is modulated by several factors, including UV irradiation, alpha‐melanocyte‐stimulating hormone ( α ‐MSH) 7, forskolin, stem cell factor (SCF) 8, wnt‐3a 9 and isobutylmethylxanthine (IBMX) 10, within intracellular melanosomes in the melanocytes 11. Stimulation of the melanocortin 1 receptor (MC1R) by α ‐MSH activates adenyl cyclase through G protein signalling, which subsequently increases cyclic adenosine monophosphate (cAMP) production.…”

Section: Introductionmentioning

confidence: 99%

Sesamol decreases melanin biosynthesis in melanocyte cells and zebrafish: Possible involvement of MITF via the intracellular cAMP and p38/JNK signalling pathways

Baek

Lee

2015

Experimental Dermatology

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The development of antimelanogenic agents is important for the prevention of serious aesthetic problems such as melasma, freckles, age spots and chloasma. The aim of this study was to investigate the antimelanogenic effect of sesamol, an active lignan isolated from Sesamum indicum, in melan‐a cells. Sesamol strongly inhibited melanin biosynthesis and the activity of intracellular tyrosinase by decreasing cyclic adenosine monophosphate (cAMP) accumulation. Sesamol significantly decreased the expression of melanogenesis‐related genes, such as tyrosinase, tyrosinase‐related protein‐1,2 (TRP‐1,2), microphthalmia‐associated transcription factor (MITF) and melanocortin 1 receptor (MC1R). In addition, sesamol also induces phosphorylation of p38 mitogen‐activated protein kinase (p38 MAPK) and c‐Jun N‐terminal kinase (JNK). Moreover, sesamol dose‐dependently decreased zebrafish pigment formation, tyrosinase activity and expression of melanogenesis‐related genes. These findings indicate that sesamol inhibited melanin biosynthesis by down‐regulating tyrosinase activity and melanin production via regulation of gene expression of melanogenesis‐related proteins through modulation of MITF activity, which promoted phosphorylation of p38 and JNK in melan‐a cells. Together, these results suggest that sesamol strongly inhibits melanin biosynthesis, and therefore, sesamol represents a new skin‐whitening agent for use in cosmetics.

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Section: Introductionmentioning

confidence: 99%

Sesamol decreases melanin biosynthesis in melanocyte cells and zebrafish: Possible involvement of MITF via the intracellular cAMP and p38/JNK signalling pathways

Baek

Lee

2015

Experimental Dermatology

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“…Numerous studies suggest that Akt inhibition is related to decreased cell growth and reduced cancer cell migration ( Sarkar and Li, 2004 ), suggesting that Akt inhibition may be an attractive approach for preventing or treating human malignancies ( Hill and Hemmings, 2002 ; Sarkar and Li, 2004 ). However, Akt activation has been implicated in cell death mediated by natural products in B16F10 murine melanoma and U373 glioblastoma cell lines ( Jin et al ., 2012 ). Thus, the roles of Akt activation and cell cycle regulation in the inhibition of cancer cell proliferation require further investigation.…”

Section: Introductionmentioning

confidence: 99%

Antitumor Effects of Fucoidan on Human Colon Cancer Cells via Activation of Akt Signaling

Han

Lee

2015

Biomolecules & Therapeutics

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We identified a novel Akt signaling mechanism that mediates fucoidan-induced suppression of human colon cancer cell (HT29) proliferation and anticancer effects. Fucoidan treatment significantly inhibited growth, induced G1-phase-associated upregulation of p21WAF1 expression, and suppressed cyclin and cyclin-dependent kinase expression in HT29 colon cancer cells. Additionally, fucoidan treatment activated the Akt signaling pathway, which was inhibited by treatment with an Akt inhibitor. The inhibition of Akt activation reversed the fucoidan-induced decrease in cell proliferation, the induction of G1-phase-associated p21WAF1 expression, and the reduction in cell cycle regulatory protein expression. Intraperitoneal injection of fucoidan reduced tumor volume; this enhanced antitumor efficacy was associated with induction of apoptosis and decreased angiogenesis. These data suggest that the activation of Akt signaling is involved in the growth inhibition of colon cancer cells treated with fucoidan. Thus, fucoidan may serve as a potential therapeutic agent for colon cancer.

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“…As tyrosinase is a critical determinant of melanin synthesis in melanocytes [41], we examined the effect of Mc-ME on tyrosinase activity and showed that Mc-ME dose-dependently suppressed tyrosinase activity in B16F10 cells (Figure 4(b)). We next examined the effect of Mc-ME on the production of melanin from melanocytes by measuring melanin content and secretion in B16F10 cells stimulated with α -MSH, which induces melanogenesis by activating melanogenesis-specific transcription factor and enzymes associated with melanin synthesis [42, 43]. As expected, Mc-ME effectively suppressed the production and secretion of melanin from melanocytes induced by α -MSH (Figures 4(c) and 4(d)).…”

Section: Discussionmentioning

confidence: 77%

Antioxidative and Antimelanogenesis Effect of Momordica charantia Methanol Extract

Park

Kim

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Despite a large number of studies reporting a variety of biological and pharmacological activities of Momordica charantia, its skin protective properties are poorly understood. The present study aimed to explore the skin protective properties of Momordica charantia methanol extract (Mc-ME) and the underlying mechanism in keratinocytes, fibroblasts, and melanocytes. Mc-ME exhibited an antioxidative property by decreasing radical levels in HaCaT keratinocytes and a cytoprotective property in H2O2-damaged HaCaT cells, which was mediated by increasing the expression or activation of Kelch-like ECH-associated protein 1 (KEAP1), HO-1, p85/PI3K, and AKT. Mc-ME was also active against wrinkle formation by regulating the activity or expression of tissue remodeling factors such as elastase, type 1 collagen, and matrix metalloproteinase (MMP)-1 and -9 and tissue-protecting enzymes such as hemeoxygenase-1 (HO-1) and sirtuin 1 (SIRT1) in NIH3T3 fibroblasts and HaCaT cells, in addition to increasing the proliferation of HaCaT cells. Mc-ME also showed antidehydration properties by inducing the expression of natural moisturizing factors such as filaggrin (FLG), transglutaminase-1 (TGM-1), and hyaluronic acid synthase (HAS)-1, -2, and -3 in HaCaT cells. Moreover, Mc-ME showed an antimelanogenic property by inhibiting the synthesis and secretion of melanin from B16F10 melanoma cells via suppression of tyrosinase activity. Taken together, these results suggest that Mc-ME plays a skin protective role through its antioxidative, cytoprotective, skin remodeling, moisturizing, and antimelanogenic properties and might be a new and promising skin protective cosmeceutical.

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Suppression of α-MSH and IBMX-induced melanogenesis by cordycepin via inhibition of CREB and MITF, and activation of PI3K/Akt and ERK-dependent mechanisms

Cited by 18 publications

References 23 publications

Sesamol decreases melanin biosynthesis in melanocyte cells and zebrafish: Possible involvement of MITF via the intracellular cAMP and p38/JNK signalling pathways

Sesamol decreases melanin biosynthesis in melanocyte cells and zebrafish: Possible involvement of MITF via the intracellular cAMP and p38/JNK signalling pathways

Antitumor Effects of Fucoidan on Human Colon Cancer Cells via Activation of Akt Signaling

Antioxidative and Antimelanogenesis Effect of Momordica charantia Methanol Extract

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