| Project/Area Number |
15K09791
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Nihon University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
照井 正 日本大学, 医学部, 教授 (30172109)
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| Co-Investigator(Renkei-kenkyūsha) |
OZAKI Toshinori 千葉県がんセンター, 研究局, 室長 (40260252)
NAGASE Hiroki 千葉県がんセンター, 研究局, 所長 (90322073)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 皮膚有棘細胞癌 / ヒストン脱メチル化酵素 / マウスモデル / 有棘細胞がん / 腫瘍関連遺伝子 / 有棘細胞癌 |
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| Outline of Final Research Achievements |
GASC1 encodes a histone demethylase which specifically demethylates lysine residues (H3K9, H3K36 and H1.4K26) and plays a crucial role in the regulation of gene expression, as well as heterochromatin formation. Recently, we have found that Gasc1-heterozygous mice (Gasc1+/-), is clearly resistant to chemically induced skin squamous cell carcinoma (SCC), indicating that Gasc1 is regulating gene(s) involved in susceptibility for SCC. Based on this result, we have conducted functional analysis of the genes differentially expressed between the skin of Gasc1+/- and wild type mice (WT), to elucidate the roles of those genes in the development and/or progression of SCC. In the present study, we have found that ZNF618, which showed significantly lower expression level in Gasc1+/- skins than those of WT, has a function to suppress cell migration ability. Detailed analysis revealed that ZNF618 could be regulated by epithelial-mesenchymal -transfer related transcription factor ZEB1.
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