| Project/Area Number |
26462425
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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 |
Urology
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
Fujii Reona 和歌山県立医科大学, 医学部, 博士研究員 (30326368)
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| Co-Investigator(Kenkyū-buntansha) |
吉川 和朗 和歌山県立医科大学, 医学部, その他 (30423940)
柑本 康夫 和歌山県立医科大学, 医学部, 准教授 (50295820)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 免疫療法 / 遺伝子免疫療法 / 癌幹細胞 / 中心体関連抗原 / Cep55/C10orf3 / survivin / 樹状細胞 / C１０0rf3（CEP55） / C100rf3（CEP55） / C10orf3（CEP55） |
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| Outline of Final Research Achievements |
Both survivin and Cep55/C10orf3 are centrosome-related genes expressed in various malignancies. Survivin, isolated as an inhibitor of the apoptosis protein family, has anti-apoptotic effects. In this study, we targeted both survivin and Cep55/C10orf3, and modified the function of dendritic cells (DC) by transducing survivin gene to DC.DC were infected with the survivin gene (DC-survivin) and Cep55/C10orf3 gene (DC-Cep55/C10orf3). DC-survivin and DC-Cep55/C10orf3 induced cytotoxic activity against T-24 and LNCaP respectively. However, cytotoxic activity against HLA non match cells (DU145) was very low. DC transduced with survivin maintained cell viability three weeks after culture, while control DC showed deterioration. By combination of two genes, survivin and Cep55/C10orf3, the cytotoxic activity against LNCaP was increased from 48 to 65%. Against T-24 it was also enhanced from 19 to 45%.This combination might offer a useful approach for the urologic cancers.
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