| Project/Area Number |
18K09533
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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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| Review Section |
Basic Section 57020:Oral pathobiological science-related
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
田沼 順一 新潟大学, 医歯学系, 教授 (20305139)
丸山 智 新潟大学, 医歯学総合病院, 講師 (30397161)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 細胞死 / 口腔がん / アポトーシス / ネクローシス / ダイイングコード / 病理学 |
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| Outline of Final Research Achievements |
Cell death through apoptosis and/or necrosis is frequently observed in malignant tumor tissues, including oral squamous cell carcinoma (OSCC). However, a significance of dead tumor cells has not been fully understood. On a hypothesis that dead tumor cells activate neighboring tumor cells and promote tumor progression, we performed the experiments using OSCC-derived cultured cells. Consequently, necrotic OSCC cells robustly activated proliferation, migration and invasion of living OSCC cells. Moreover, necrotic OSCC cells induced activation of NF-kB pathway and increased production of inflammatory cytokines. Our study demonstrated dead tumor cell-induced cellular activation mechanisms in OSCC.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の結果から、腫瘍組織内で生じた死細胞が増殖・遊走・浸潤といった細胞活性化の起点となること、さらに分子機序としてToll-like受容体およびNF-kB経路の関与が明らかとなった。本研究の成果は、化学放射線療法後の腫瘍再発メカニズムの解明に寄与するとともに、新規制癌治療法の開発につながる可能性がある。
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