| Project/Area Number |
17K16857
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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 | Oita University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2020: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | miR-100 / SMARCD1 / Mir-100 / MMP1 / 標的遺伝子 / MMP-1 / マイクロアレイ |
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| Outline of Final Research Achievements |
Using miR-100, which is upregulated in endometriosis, we investigated whether normal endometrial stromal cells express the characteristic traits of endometriosis. As a result, it was discovered that SMARCD1 and MMP1 are related to the signal pathway downstream of miR-100. In this study, it was found that miR-100 activates MMP1 by inhibiting SMARCD1 and enhances the migration and infiltration ability of normal endometrial stromal cells. These findings suggest that enhanced miR-100 expression in endometriosis is involved in promoting the acquisition of endometriosis-specific characteristics during endometriosis development. Our present findings on the roles of miR-100 may thus contribute to understand the epigenetic mechanisms involved in the pathogenesis of endometriosis．
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| Academic Significance and Societal Importance of the Research Achievements |
現在の子宮内膜症の治療はホルモン療法が主体であり、効果はあるものの副作用の観点、また不妊治療には適さないなど問題がある。今回の研究において遺伝子レベルでの子宮内膜症の病態の一端を解明することができた。これにより子宮内膜症の病態に焦点を合わせた新たな治療薬の開発が見いだせる可能性が示唆された。
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