| Project/Area Number |
16K10493
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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 |
Digestive surgery
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
太田 哲生 金沢大学, 医学系, 教授 (40194170)
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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 |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 食道発癌 / 逆流性食道炎 / がん微小環境 / 化学予防 / エピジェネティック / メトホルミン / 癌 |
|---|
| Outline of Final Research Achievements |
Recently, metformin has been reported to be an anti-inflammatory, inhibition of phospho-Stat3 and antitumor activity. We evaluated that the dynamic alterations of infiltrating immune cells in esophageal carcinogenesis and investigated the anti-cancer effects of metformin.
Flow cytometric analysis demonstrated that the balance of M1- and M2-polarized macrophages, as well as the number of phospho-Stat3-positive macrophages, regulatory T cells, cytotoxic T cells, and natural killer cells, were dynamically changed at each stage of the disease. Metformin treatment stimulated immunomodulation at every stage. Overall, these findings suggest that metformin suppressed the esophageal carcinogenesis by improving the immunosuppressive tumor microenvironment.
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| Academic Significance and Societal Importance of the Research Achievements |
Ⅱ型糖尿病治療薬であるメトホルミンが癌組織を構築する抑制性免疫細胞の浸潤を抑制することにより癌微小環境を改変し、発癌抑制作用を有する可能性が示唆された。がん微小環境に対する既存薬再開発（ドラッグリポジショニング）につながる研究の成果と思われる。
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