| Project/Area Number |
25461705
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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 | Sapporo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
鈴木 拓 札幌医科大学, 医学部分子生物学講座, 教授 (20381254)
肥田 時征 札幌医科大学, 医学部皮膚科学講座, 講師 (90464487)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 悪性黒色腫 (メラノーマ) / インターフェロン-β / アポトーシス / DNAメチル化 / 5-aza-2’-cytidine / microRNA (miR) / 次世代シーケンス / インターフェロンbeta / 5-aza-2'-cytidine / ドライバー変異 / インターフェロン-β (INF-β) / メチル化 / microRNA (miRNA) |
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| Outline of Final Research Achievements |
We aimed to examine the epigenetically silenced miRNA and its involvement in the induction of apoptosis of cultured melanoma cells. A screen for miRNAs induced by 5-aza-2’deoxycytidine (5-aza-dC) and interferon-beta (IFN-β) in TXM18 melanoma cells identified six species of miRNAs including miR-7, miR-203, miR-215 and miR-596. The CpG island of the miR-596 gene was strongly methylated in all melanoma cell lines tested (n = 20) whereas methylation levels were limited in melanocytes (n=4). Transfection of a precursor of miR-596 into melanoma cells induced growth suppression, indicating that the effect of 5-aza-dC plus IFN-β is in part due to induction of miR-596. Methylation levels of miR-596 were significantly higher in clinical specimens of melanoma as compared to benign melanocytic nevi.
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