| Project/Area Number |
17K16781
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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 | The University of Tokyo |
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Principal Investigator |
Yamada Yuta 東京大学, 医学部附属病院, 登録診療員 (10376452)
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 腎癌 / TRIM / ユビキチン / TRIM44 / ユビキチン化 / 癌 / 遺伝子 / tripartite motif |
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| Outline of Final Research Achievements |
We investigated the clinical significance of TRIM44 and its biological function in RCC. TRIM44 overexpression was also significantly associated with cancer specific survival. Functional studies using TRIM44 cDNA and siTRIM44 transfection revealed that TRIM44 promotes cell proliferation and cell migration in Caki1 and 769P cells. We then performed integrated microarray analysis in Caki1 and 769P cells and explored the data in the Oncomine database. fyn-related kinase (FRK) was identified as the promising candidate target gene of TRIM44, which was downregulated in RCC compared with normal renal tissues. We revealed that cell proliferation was inhibited by TRIM44 knockdown and then recovered by siFRK supplement. Taken all together, this study showed the association between TRIM44 overexpression and poor prognosis in RCC patients, and that TRIM44 facilitated cell proliferation by regulating FRK.
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| Academic Significance and Societal Importance of the Research Achievements |
腎癌の新規治療ターゲットになりえる分子TRIM44を同定した。
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