| Project/Area Number |
25462045
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
Motoi Fuyuhiko 東北大学, 医学系研究科, 准教授 (30343057)
Fukase Koji 東北大学, 大学病院, 助教 (00578677)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | GCF2 / LRRFIP1 / EMT / Wnt signal / 膵癌 / β-catenin / Wnt / 上皮間葉移行 / Wntシグナル |
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| Outline of Final Research Achievements |
The canonical Wnt/β-catenin signaling pathway has been shown to promote the epithelial-mesenchymal transition (EMT), which is a crucial process in multiple embryonic developmental processes and the progression of carcinomas. In the present study, we identified the signaling elements targeted by GCF2 for promotion of the EMT in pancreatic cancer. GCF2 silencing reversed the EMT, as shown by increased expression of E-cadherin (an epithelial marker) and decreased expression of vimentin (a mesenchymal marker). Silencing of GCF2 up-regulated phosphorylation of β-catenin and decreased its nuclear localization by targeting β-catenin destruction complex. The migration and invasion capabilities were strongly inhibited in GCF2 knocked down pancreatic cancer cells. Consequently, our data strongly suggested that LRRFIP1 played an important role in the invasion of carcinoma cells and as an attractive candidate for targeted therapy in human cancers.
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