| Project/Area Number |
26861292
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Urology
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| Research Institution | National Cancer Center Japan (2015)
Saitama Medical University (2014) |
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Principal Investigator |
Miyazaki Toshiaki 国立研究開発法人国立がん研究センター, がん分化制御解析分野, 研究員 (50589075)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | EBAG9 / がん / 微小環境変化 / 腫瘍免疫 / Cancer / がん微小環境 / がん腫瘍免疫 / 泌尿器がん |
|---|
| Outline of Final Research Achievements |
EBAG9 overexpression is found in several cancers and correlated with poor prognosis of patients with the cancers; however, the mechanism is not fully understood. In this study, tumor growth of mouse bladder cancer cells subcutaneously inoculated into Ebag9 knockout (Ebag9KO) mice was found to be suppressed compared with that of control mice. Tumor metastasis in lung was also suppressed in Ebag9KO mice. Furthermore, the number of T cell infiltration was increased in implanted tumors of Ebag9KO mice. We also found that the CD8+ T cells exhibited upregulation of cytotoxic activity, and the adoptive transfer of CD8+ T cells isolated from tumors in Ebag9KO host could repress tumor growth by mouse bladder cancer cells implanted in wild-type host. Gain and loss-of-function analysis of EBAG9 demonstrated that EBAG9 modulates migration in prostate cancer cells. These results suggest that EBAG9 modulates tumor growth by negatively regulating the adaptive immune response in host defense.
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