2014 Fiscal Year Final Research Report
oncomir and its target gene in endometrial carcinogenesis
| 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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| Keywords | endometrial cancer / micro RNA / miR-31 / LATS2 / hippo pathway |
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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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| Free Research Field |
婦人科腫瘍学
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