| Project/Area Number |
17K11684
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Meikai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
廣井 美紀 明海大学, 歯学部, 講師 (30419717)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ケモカイン / CXCL11 / CD4 / CD8 / F4/80 / CD163 / CXC11 / CD31 / Perforin / IFN / 扁平上皮癌 / マクロファージ / 前癌病変 |
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| Outline of Final Research Achievements |
To investigate the antitumor activity of interferon-inducible chemokines, we established stable cell lines transfected with expression vectors of CXCL9 (Mig), CXCL10 (IP-10), and CXCL11 (I-TAC) into the mouse squamous cell carcinoma cell line, SCCVII, and examined the effect of these chemokine-expressing cell lines on tumorigenesis after transplantation into nude mice. These results indicate that CXCL9 and CXCL11 suppressed tumor growth via the cytotoxic effect of infiltrated NK cells and growth inhibitory effect of vascular endothelial cells. In addition, infiltration of F4/80-positive cells was suggested to be involved in the suppression of tumorigenesis.
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| Academic Significance and Societal Importance of the Research Achievements |
白板症部はTh1優位な微少環境であり、ケモカインCXCL9によって浸潤したTh1がIFNγを産生し、CD163+ M1 マクロファージの分化誘導に関与していることが示唆された。このように上皮性異形成から癌腫へと進行するいわゆるdysplasia-carcinoma sequenceの経緯のなかで、マクロファージは発癌においてどのような役割があるかについて明らかにすることは、臨床的に発癌の前段階において疾患を予測する診断マーカーの確立および発癌予防に寄与するものとして大変意ある検討と考え本研究課題を申請した。
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