| Project/Area Number |
15K20128
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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 |
Obstetrics and gynecology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Sone Kenbun 東京大学, 医学部附属病院, 助教 (90598872)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | エピジェネティクス / 子宮体癌 / 卵巣癌 / メチル化 / 脱メチル化 / ヒストンメチル化酵素 / ＥＺＨ２ / ヒストン脱メチル化酵素 / EZH2 / SUV420H1 |
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| Outline of Final Research Achievements |
We investigated the involvement of histone methyltransferase and demethylase in ovarian cancer and endometrial cancer and evaluated its therapeutic potential. At first, we investigated the expression and function of histone methyltransferase EZH2 in endometrial cancer. In a quantitative real-time PCR analysis of 11 endometrial cancer cell lines and 52 clinical endometrial cancer specimens, EZH2 was significantly overexpressed in cancer cells and tissues compared to that in normal control cells and tissues. In addition, knockdown of EZH2 using specific siRNAs resulted in growth suppression and apoptosis induction of endometrial cancer cells. Consistent with these results, treatment with a specific EZH2 inhibitor, suppressed endometrial cancer cell growth. Further studies should explore the therapeutic potential of inhibiting EZH2 in patients with endometrial cancer.
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