| Project/Area Number |
26861050
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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 |
General surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
MASUDA Toshiro 熊本大学, 医学部附属病院, 非常勤診療医師 (50551256)
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| Research Collaborator |
NAKAGAWA Shigeki 熊本大学, 医学部附属病院, 非常勤診療医師 (10594872)
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | HCC / micro RNA / EZH2 / Cancer progression / 肝細胞癌 / マイクロRNA / 細胞周期 / Zeste Homolog 2 |
|---|
| Outline of Final Research Achievements |
Previously we reported that the EZH2 (Enhancer of Zeste Homolog 2) regulate cancer progression. Here, we retrieved microRNAs which regulate the EZH2 expression from the database of HCC (Hepatocellular carcinoma) cell lines, and we identified miR-32 and miR-382. We analyzed how miR-EZH2 pathway worked in HCC progression, and we found that the pathway suppressed p16INK4a and CDH1. p16INK4a is known as tumor suppressor gene and regulate cell cycle and senescence, and CDH1 is known as a EMT (Epithelial-Mesenchymal Transition) marker and suppress EMT.
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