Notch signaing promotes proliferation and migration of melanoma.
| Project/Area Number |
25461689
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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 | Shinshu University |
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Principal Investigator |
KINIWA Yukiko 信州大学, 学術研究院医学系(医学部附属病院), 講師 (20436893)
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| Co-Investigator(Kenkyū-buntansha) |
OKUYAMA Ryuhei 信州大学, 学術研究院医学系, 教授 (80292332)
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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: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | メラノーマ / Notchシグナル / DELTA-like 3 / MAPK経路 / Notchシグナリング / Notchリガンド |
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| Outline of Final Research Achievements |
Background: Notch signaling is crucial for development and cell differentiation in various tissues. It is also elucidated to be important in tumorigenesis. There are four Notch receptors (Notch1~4) and five ligands [Delta-like (DLL) 1/3/4 and Jagged 1/2] in Notch signaling pathway. Notch1 has been reported to be oncogenic in melanoma. However, little is known about importance of the ligands. In this study, we tried to determine the role of DLL3 in progression of melanoma.
Results: DLL3 was preferentially expressed in melanoma rather than melanocytic nevus. HES1 expression was decreased by DLL3-knockdown using specific siRNA, showing that DLL3 contributes to Notch signaling pathway. DLL3-knockdown decreased cell proliferation and migration. DLL3-knockdown led G0/G1 arrest, and suppressed MAPK signaling pathway. DLL3 overexpression increased cell proliferation and migration. These findings provided insight into the role of DLL3 in melanoma progression through MAPK activation.
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Report
(4 results)
Research Products
(8 results)
