ArticleScientific reports2019
TNFα-signal and cAMP-mediated signals oppositely regulate melanoma- associated ganglioside GD3 synthase gene in human melanocytes.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 7 citations in OpenAlex.
- Dietary Lipids and Lipid-Mediated Signaling Neurovascular Unit Dysfunction: Implications for Alzheimer's and Parkinson's Diseases Pathogenesis.Molecular neurobiology · 2026Review
- Ganglioside Expression in Melanocytes: Modulation by Intrinsic and Extrinsic Factors.Methods in molecular biology (Clifton, N.J.) · 2026Article
- GD2 is a Crucial Ganglioside in the Signal Modulation and Application as a Target of Cancer Therapeutics.Cancer science · 2025Review
- An overview of benefits and risks of chronic melanocortin-1 receptor activation.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Review
- Ganglioside GD3 Regulates Inflammation and Epithelial-to-Mesenchymal Transition in Human Nasal Epithelial Cells.International journal of molecular sciences · 2024Article
- Antitumor Properties of Epitope-Specific Engineered Vaccine in Murine Model of Melanoma.Marine drugs · 2022Article
- Multiplicity of Glycosphingolipid-Enriched Microdomain-Driven Immune Signaling.International journal of molecular sciences · 2021Review
- Antiganglioside Antibodies and Inflammatory Response in Cutaneous Melanoma.Journal of immunology research · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Analyses of expression and regulation of ganglioside synthases in melanocytes are important to understand roles of gangliosides in melanomagenesis. In this study, we analyzed the expression and regulatory mechanisms of glycosyltransferase genes responsible for ganglioside synthesis in normal melanocytes. We reported previously that culture supernatants of UVB-irradiated keratinocytes induced upregulation of ganglioside GD3 synthase gene in melanocytes, and mainly TNFα was responsible for it. Then, we found that elimination of dibutyryl cyclic AMP and IBMX from the medium also resulted in upregulation of the GD3 synthase gene. The addition of α-melanocyte-stimulating hormone which increases cAMP, to the medium led to a significant reduction in the GD3 synthase gene expression level, and a PKA inhibitor enhanced the GD3 synthase gene level. These results suggest that signals mediated via TNFα and cAMP oppositely regulate GD3 synthase gene expression in melanocytes. The results of an IKK inhibitor indicate the possibility that TNFα induces GD3 synthase gene expression via NF-κB signaling in melanocytes. When melanoma cells were treated by these factors, no fluctuation in the GD3 synthase gene expression level was observed, although an IKK inhibitor significantly suppressed it, suggesting that ganglioside synthase genes are regulated in distinct manners between melanocytes and melanomas.
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