Project/Area Number |
21592120
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
|
Research Institution | Tohoku University |
Principal Investigator |
NAGASE Satoru 東北大学, 大学院・医学系研究科, 准教授 (00292326)
|
Co-Investigator(Kenkyū-buntansha) |
大槻 健郎 東北大学, 病院, 助教 (40531330)
岡本 聡 東北大学, 病院, 臨床検査技師 (40420020)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
Keywords | 子宮体癌 / 子宮体部漿液性腺癌 / 類内膜腺癌 / マイクロRNA / 発現プロファイル / 子宮体がん / 標的遺伝子 |
Research Abstract |
We compared miRNA expression levels in uterine papillary serous carcinoma (UPSC)with the levels in endometrial endometrioid adenocarcinoma (EEC)and normal endometria. Eight miRNAs were identified as having aberrant down-regulation specific to UPSC with miR-34b being most pronounced. Ectopic expression of miR-34b inhibited cell growth, migration, and most notably invasion. These effects are likely mediated by the downstream target of miR-34b, the proto-oncogene MET, a known prognostic factor in endometrial carcinomas. The expression of MET was reduced following the restoration of miR-34b in cell lines. In summary, our data suggest that miR-34b plays a role in the molecular pathogenesis of ESC.
|