Elucidation of mechanisms of pancreatic cancer lymphangiogenesis
| Project/Area Number |
16K19947
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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 |
Digestive surgery
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| Research Institution | Nagoya City University |
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Principal Investigator |
Saito Kenta 名古屋市立大学, 大学院医学研究科, 助教 (10770240)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 膵癌 / リンパ管新生 / K-ras mutation / ,VEGF-C / VEGF-C |
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| Outline of Final Research Achievements |
In order to elucidate the mechanism of lymph node metastasis of pancreatic cancer (PaCa), the following study was conducted. Pancreatic cancer cell lines were classified into VEGF-C strong expression strains and VEGF-C low expression strains. PaCa with high VEGF-C enhanced the invasive ability and tube formation of lymphatic endothelial cells compared with PaCa with weak VEGF-C. In addition, focusing on K-ras mutation, PaCa with K-ras mutation showed higher lymphangiogenesis potential than K-ras wild. The suppression of VEGF-C / VEGF-R3 (VEGF-C receptor) signal reduced the enhanced lymphangiogenesis by PaCa. So these results suggested that this signal may contribute to PaCa lymphangiogenesis and might become a new therapeutic target.
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Report
(3 results)
Research Products
(17 results)
