| Project/Area Number |
25462466
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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 | Akita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Takamitsu 秋田大学, 医学部, 講師 (60375243)
HUANG Mingguo 秋田大学, 医学部, 助教 (60448503)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 前立腺癌 / microRNA / 高脂肪食 / MET / miR-130a |
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| Outline of Final Research Achievements |
We assessed the roles of altered miRNAs in HFD-induced PCa progression. We found 59 up- and down-regulated miRNAs in xenografts under the HFD condition using microRNA Array analysis. In those miRNAs, we focused on miR-130a because of the expression levels with significantly lower in three PCa cells. In ex vivo, PCa cells cultured in medium containing HFD-fed mouse serum had significantly higher cell proliferation with lower expression levels of miR-130a. The PCa cells transfected with miR130a down-regulated MET, AR and DICER1, and MET expression was higher in HFD-induced PCa models. In human tissues, the mean miR-130a expression level of cancer epithelia was significantly lower than that of normal epithelia, and cytoplasmic MET in PCa tissues overexpressed in patients with higher BMI. In conclusion, a substantial number of miRNAs altered in HFD-induced PCa growth. In particular, miR-130a/MET pathway was associated with HFD-induced PCa progression.
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