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2015 Fiscal Year Final Research Report

The relationship between microenvironment and tumor growth mechanism regulated by EBAG9 in urological cancer and the application to clinical

Research Project

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Project/Area Number 26861292
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Urology
Research InstitutionNational Cancer Center Japan (2015)
Saitama Medical University (2014)

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)

Project Period (FY) 2014-04-01 – 2016-03-31
KeywordsEBAG9 / がん / 微小環境変化 / 腫瘍免疫
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.

Free Research Field

医歯薬学

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Published: 2017-05-10  

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