| Project/Area Number |
19590728
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Nagasaki University |
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Principal Investigator |
ISOMOTO Hajime Nagasaki University, 病院, 准教授 (90322304)
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| Project Period (FY) |
2007 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2009: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2008: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | Mcl-1 / STAT3 / microRNA / epigenetics / SOCS3 / microRNA-205 / microRNA-10a / 上皮間葉転換 / squamous cell carcinoma / esophagus / micro RNA / miR-205 / miR-29b / 食道扁平上皮癌 / stat3 / IL-6 / miRNA-205 / JAK |
|---|
| Research Abstract |
We sought to identify esophageal squamous cell carcinoma (SCC) specific microRNA (miR) to elucidate regulatory mechanisms of Mcl-1. RNA from SCC cell lines, immortalized non-malignant SC cell and various malignant cells was subjected to miR microarray. The candidate miRs were analyzed by quantitative RT-PCR. MiR-205 can be specifically upregulated in the SCC. As for its function, miR-205 was associated with migration capacity with Matrigel assay, but not with proliferation, apoptosis and wound healing, when assessed by cellular transfection of its precursor or inhibitor. On the other hand, miR-10a was substantially downregulated in the SCC, and could be restored by treatment with 5-azadeoxycytidine and/or trichostatin A.
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