Elucidation of the role of Interleukin-32 involved in the invasive process of pancreatic cancer and its expression mechanism.
| Project/Area Number |
16K08707
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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 |
Experimental pathology
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| Research Institution | University of Toyama |
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Principal Investigator |
Imura Johji 富山大学, 大学院医学薬学研究部(医学), 教授 (80316554)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 膵癌 / 浸潤 / IL-32 / 細胞株 / Interleukin-32 / サイトカイン |
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| Outline of Final Research Achievements |
This study was performed to investigate the invasiveness regulating factors that defines poor prognosis for pancreatic cancer. First, a highly invasive cell was established from the human-derived pancreatic cancer cell lines. IL-32 has been highly enhanced among several genes to expression. Furthermore it was confirmed whether IL-32 was involved in invasiveness. It was found that the invasiveness was inhibited by siRNA for IL-32, and the invasiveness was obtained when IL-32 was forcibly expressed in non-invasive cell. In pancreatic cancer tissues, the expression of IL-32 was not appeared in normal pancreatic ducts, was expressed in tumor cells, and it was particularly enhanced in the infiltrating area. The factors regulated by IL-32 were involved E-Cadherin, MMP4・14・9, Thrombospondin 1, Slug, BMP4 and etc.
From the above, it was suggested that IL-32 may be an important factor involved not only in inflammation but also in the invasiveness of pancreatic cancer.
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| Academic Significance and Societal Importance of the Research Achievements |
膵癌は最近、死亡率が増加の一途を辿っている。何故に、膵癌が予後不良なのか？その原因は数々あるが、特に膵癌は容易に周辺臓器に浸潤し易く、手術不能となることも要因である。では、なぜに易浸潤性なのか？浸潤を制御している機構や分子はどの様なものがあるのか？それらを明らかにすることが本研究の目的である。まず、浸潤性の高い細胞を作成し、これらで高発現している分子の中からL-32を見出した。さらに、IL-32を減少させると浸潤性が減弱し、亢進させると浸潤性を増すことを確認した。また、IL-32によって制御を受ける分子も明らかにした。今後、IL-32と共に、他の分子を抑制するような創薬にも繋がる研究である。
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Report
(4 results)
Research Products
(12 results)
