| Project/Area Number |
16K20168
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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 |
Obstetrics and gynecology
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| Research Institution | Hokkaido University |
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Principal Investigator |
Nakagawa Hisako 北海道大学, 遺伝子病制御研究所, 特任助教 (60615342)
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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 |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Be-ta 2 Glycoprotein / 乳がん / 腫瘍転移 / EGF / Beta 2 Glycoprotein / EGFR / Beta-2-Glycoprotein I / 蛋白質 / 血管新生 / 乳癌 |
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| Outline of Final Research Achievements |
To investigate the significance and functional role of B2GPI in angiogenesis and cancer invasion/metastasis, VE-cadherin endocytosis assay was performed in the presence or absence of intact or nicked B2GPI using HUVECs. We found that B2GPI and nicked B2GPI inhibit VE-cadherin endocytosis and cell permeability. The proliferation of tumor cells was inhibited and F-actin polymerization was suppressed by only intact form B2GPI. In addition, B2GPI suppressed the EGF-EGFR interaction, such as EGFR2 phopholyration and nuclear tracslocation.In general, Epithelial-Mesenchymal Transformation (EMT), as it is associated with cell proliferation, differentiation and migration, is induced by growth factor. We investigated that the influence of B2GPI for EMT. The mRNA expression levels and protein levels of EMT related transcription factors Slug, Snail and Vimentin were down-regulated after B2GPI treatment. These data suggest that B2GPI is a critical novel regulator for angiogenesis and tumorigenesis.
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