The elucidation of the mechanism by which DYRK2 expression is regulated
| Project/Area Number |
26861056
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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 | Jikei University School of Medicine |
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Principal Investigator |
Mimoto Rei 東京慈恵会医科大学, 医学部, 助教 (70710333)
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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: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 乳癌 / DYRK２ / DYRK2 / エベロリムス / リン酸化酵素 / キーノード解析 / 翻訳後修飾 |
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| Outline of Final Research Achievements |
Our recent study revealed that DYRK2 has a tumor-suppressive function through c-Myc, c-Jun, and Snail expression and phosphorylation of p53. DYRK2 expression is decreased in advanced breast cancer and serous ovarian cancer. Diminished expression of DYRK2 confers drug-resistance to cytotoxic chemotherapy and poor prognosis in these cancers. However, the therapeutic strategy has not been established for breast cancer patients with low DYRK2 expression. Through microarray analysis, mTORC1 pathway was detected as the activated pathway in DYRK2 depleted cells. mTOR inhibitor, everolimus treatment was associated with a significant inhibition of tumor growth compared to vehicle in vitro and in vivo.
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Report
(3 results)
Research Products
(2 results)
