| Project/Area Number |
22591773
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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 |
Urology
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
ISHIBASHI Kei 福島県立医科大学, 医学部, 講師 (90347211)
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| Co-Investigator(Kenkyū-buntansha) |
SHISHIDO Keiichi 福島県立医科大学, 医学部, 博士研究員 (30285035)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 腫瘍学 / 腎癌 / インターフェロン / IL-6 / SOCS3 / miRNA |
|---|
| Research Abstract |
Interferon (IFN)-α is one of the most commonly used agents in immunotherapy for patients with advanced -stage renal cell carcinoma. However, because of the drug resistance to IFN-α, its benefits are limited. In this study, we evaluated theexpression of hsa-miR-93 or SOCS3-mRNA in renal cell carcinoma cells which resists to IFN treatment. Among the renal cell carcinoma cell lines which we used in this study, 786-O cells showed resistance to IFN treatment. The expression of both hsa-miR-93 and SOCS3-mRNA was significantly higher compared with other cell lines. Suppression of hsa-miR-93 or SOCS3-mRNA induced sensitivity to IFN in 786-O cells. Especially, down regulation of SOCS3-mRNA enhanced STAT1 activation and anti-tumor activity of IFN, both in vitro and in vivo, in a human IFN- resistant RCC cell line 786-O. Because IL-6 receptor antibody blocked SOCS3 efficiently, combination therapy using an antihuman IL-6R antibody with IFN-α may represent a novel therapeutic approach for the treatment of renal cell carcinoma.
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