| Project/Area Number |
25670690
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | endometrial cancer / micro RNA / miR-31 / LATS2 / hippo pathway / microRNA / hippo signaling pathway / cyclinD1 / microRNA-31 |
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| Outline of Final Research Achievements |
The overexpression of microRNA-31 (miR-31) significantly promoted anchorage-independent growth in vitro and significantly increased the tumor forming potential in vivo in endometrial cancer cells. miR-31 significantly suppressed the luciferase activity of mRNA combined with the LATS2 3’-UTR and consequently promoted the translocation of YAP1, a key molecule in the Hippo pathway, into the nucleus. Meanwhile, the nuclear localization of YAP1 increased the transcription of cyclinD1. Furthermore, the expression levels of miR-31 were significantly increased in the patients (n = 27) with a high risk of recurrence compared to that observed in the low-risk patients (n = 7), and this higher expression correlated with a poor survival.
We conclude that miR-31 functions as an oncogene in endometrial cancer by repressing the hippo pathway. miR-31 is a potential new molecular marker for predicting the risk of recurrence and prognosis of endometrial cancer.
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