UVB-irradiated keratinocytes induce melanoma-associated ganglioside GD3 synthase gene in melanocytes via secretion of tumor necrosis factor α and interleukin 6

Miyata, Maiko; Ichihara, Masatoshi; Tajima, Orie; Sobue, Satoshi; Kambe, Mariko; Sugiura, Kazumitsu; Furukawa, Koichi

doi:10.1016/j.bbrc.2014.02.038

Cited by 20 publications

(27 citation statements)

References 38 publications

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“…Transcriptional factor NF-B has been reported to be one of the regulators for the expression of GD3 synthase gene in human cells (42). Tumor necrosis factor ␣ and interleukin 6 enhanced the expression of GD3 synthase in melanocytes (43), suggesting the involvement of NF-B. It is also known that there are correlations between NF-B activation and poor prognosis in gliomas (44).…”

Section: Discussionmentioning

confidence: 99%

Ganglioside GD3 Enhances Invasiveness of Gliomas by Forming a Complex with Platelet-derived Growth Factor Receptor α and Yes Kinase

Ohkawa

Momota

Kato

et al. 2015

Journal of Biological Chemistry

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Background: Roles of GD3 in gliomas are not well understood. Results: PDGF receptor ␣ was identified as a GD3-associated molecule by enzyme-mediated activation of radical sources and mass spectrometry, and its association with GD3 and Yes leads to increased invasiveness. Conclusion: GD3 enhances invasiveness by forming a molecular complex. Significance: GD3/PDGF receptor ␣⅐Yes complex is a potential target for glioma therapy.

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Section: Discussionmentioning

confidence: 99%

Ganglioside GD3 Enhances Invasiveness of Gliomas by Forming a Complex with Platelet-derived Growth Factor Receptor α and Yes Kinase

Ohkawa

Momota

Kato

et al. 2015

Journal of Biological Chemistry

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“…GD3 has been also considered as melanoma-associated gangliosides [85]. Recently, we have found that inflammatory cytokines such as TNFa and interleukin 1b secreted from UVB-irradiated keratinocytes induced GD3 expression on normal melanocytes [86]. These findings suggest that induced neo-GSLs due to stimulations and/or under inflammatory reaction play roles in the modulation of host responses, and induction of solid changes in the phenotypic and genetic/epigenetic states during long-term chronic inflammation.…”

Section: Gsls Are Regulated During Inflammatory Reactions and May Be mentioning

confidence: 96%

Regulatory function of glycosphingolipids in the inflammation and degeneration

Ohmi¹,

Ohkawa²,

Tajima³

et al. 2015

Archives of Biochemistry and Biophysics

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“…Induction of GD3 synthase gene and suppression of GM1/GD1b synthase in melanocytes as measured by qRT-PCR. Melanocytes were cultured for 2 days with the supernatant of HaCat cells that had been exposed to repeated UV irradiation, and gene expression was analyzed by qRT-PCR [26]. Cells cultured with fresh medium were used as controls (NC).…”

Section: Journal Of Clinical and Cellular Immunologymentioning

confidence: 99%

“…Here, what we are most interested in is that melanocytes did not respond to UVB exposure in terms of cytokine production and secretion [26], although they might undergo DNA damage by UVB. Consequently, keratinocytes responded to UVB exposure by secreting various cytokines such as TNFα, IL-6, IL-1β, and IL-8 etc.…”

Section: Introductionmentioning

confidence: 99%

“…Consequently, keratinocytes responded to UVB exposure by secreting various cytokines such as TNFα, IL-6, IL-1β, and IL-8 etc. Furthermore, the fact that these cytokines secreted from UV-irradiated keratinocytes induced expression of melanoma-associated ganglioside GD3 on melanocytes [26]. Culture supernatants from those keratinocytes also suppressed GM1/GD1b synthase gene in melanocytes, that is now considered to be rather a suppressive antigen…”

Section: Introductionmentioning

confidence: 99%

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Inflammatory Reactions in Microenvironments, Leading to Melanomagenesis

Miyata¹,

Kambe²,

Takeuchi³

et al. 2017

J Clin Cell Immunol

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Malignant melanoma is resistant to various therapies, while its incidence has been dramatically increasing. Among various factors, sun exposure, particularly ultra violet (UV) irradiation is considered to induce melanomas. Gangliosides have been markers of neuro-ectoderm-derived cancers like malignant melanomas and gliomas, but they also play crucial roles in their malignant properties. GD3 regulates cell signalling transduced through membrane microdomains. Chronic inflammatory reactions toward noxious stimuli cause cumbersome diseases such as cancers and degeneration, and glycosylation is involved in those processes. Here, melanocytes did not respond to UVB, while keratinocytes responded to UVB by secreting various cytokines such as TNFα and IL-6. Furthermore, these cytokines induced expression of melanoma-associated ganglioside GD3 on melanocytes. Expression of GD3 does not necessarily induce melanomas, but may form microenvironments for the generation of melanomas after longterm continuation. Consequently, combination of DNA mutagenesis and chronic inflammatory reaction seems to be critical for the melanomagenesis. Thus, 1. Mechanisms for the induction of GD3 synthase gene by inflammatory cytokines. 2. Meaning of GD3 expression in melanocytes. 3. Linkage between GD3 expression in melanocytes and melanomagenesis. 4. Prevention of UV exposure, are proposed as urgent issues to be solved in the near future.

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UVB-irradiated keratinocytes induce melanoma-associated ganglioside GD3 synthase gene in melanocytes via secretion of tumor necrosis factor α and interleukin 6

Cited by 20 publications

References 38 publications

Ganglioside GD3 Enhances Invasiveness of Gliomas by Forming a Complex with Platelet-derived Growth Factor Receptor α and Yes Kinase

Ganglioside GD3 Enhances Invasiveness of Gliomas by Forming a Complex with Platelet-derived Growth Factor Receptor α and Yes Kinase

Regulatory function of glycosphingolipids in the inflammation and degeneration

Inflammatory Reactions in Microenvironments, Leading to Melanomagenesis

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