| Project/Area Number |
26462399
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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 | University of Tsukuba |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
宮崎 淳 筑波大学, 医学医療系, 准教授 (10550246)
末富 崇弘 筑波大学, 医学医療系, 講師 (10574650)
西山 博之 筑波大学, 医学医療系, 教授 (20324642)
神鳥 周也 筑波大学, 医学医療系, 助教 (50707825)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 腎細胞癌 / 低分子量Gタンパク / 肉腫様腎細胞癌 / 肉腫様変化 |
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| Outline of Final Research Achievements |
We evaluated the expression of VAV1 in samples of patient with clear cell renal cell carcinoma (ccRCC) by Quantitative RT-PCR. The mRNA expressions of VAV1 were elevated in ccRCC. However, cell proliferation and invasion were not suppressed by VAV1 knockdown in renal cancer cell lines. Therefore, we next focused on PLD2 as the guanine nucleotide exchange factor of RAC2. We evaluated the expression of PLD2 in samples of patient with ccRCC by immunohistochemical staining. The high expression of PLD2 was significantly associated with a poorer prognosis in patients with ccRCC. Moreover, cell proliferation and invasion were suppressed by PLD2 knockdown in renal cancer cell lines. These results suggest that PLD2 may become a new target of therapy for ccRCC.
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