| Project/Area Number |
15K08346
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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 |
Human pathology
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| Research Institution | Kochi University |
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Principal Investigator |
FURIHATA Mutsuo 高知大学, 教育研究部医療学系連携医学部門, 教授 (10209158)
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| Co-Investigator(Kenkyū-buntansha) |
谷内 恵介 高知大学, 医学部附属病院, 特任准教授 (50626869)
岩崎 信二 高知大学, 教育研究部医療学系臨床医学部門, 准教授 (10232654)
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| Project Period (FY) |
2015-10-21 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 膵癌 / 浸潤転移 / RNA結合蛋白 / RNA結合蛋白RNA / 免疫組織化学 / RNA結合蛋白 RNA / RNA結合蛋白 RNA |
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| Outline of Final Research Achievements |
We previously reported that mRNA-binding protein-bound transcripts accumulate in membrane protrusions of pancreatic ductal adenocarcinoma (PDAC) cells, and the formation of additional membrane protrusions increased the invasive and metastatic properties of the PDAC cells. In the course of this investigation, we picked up the three mRNA-binding proteins; Var3, PODXL and CCDC88, and demonstrated that these candidate markers were accumulated in cell protrusions, contributed to the formation of membrane protrusions, and increased the migration and invasiveness of PDAC cells. In contrast, knockdown of each of them inhibited the motility and invasiveness of PDAC. Immunohistochemistry leveled that high expression of these proteins was an independent predictor of worse overall survival of pancreatic cancer patients. Our studies suggest that they can be a useful marker for predicting the outcome of patients with PDAC and thereby increased the motility and invasiveness of PDAC.
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