| Project/Area Number |
16K10482
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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 |
General surgery
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| Research Institution | Osaka Medical College |
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Principal Investigator |
ITO YUKO 大阪医科大学, その他部局等, 功労教授 (40148432)
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| Co-Investigator(Kenkyū-buntansha) |
柴田 雅朗 大阪医科大学, 医学部, 准教授 (10319543)
Eid NabilA.S. 大阪医科大学, 医学部, 講師 (50570165)
濱岡 仁美 (黒瀬仁美) 大阪医科大学, 医学部, 講師 (80545608)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 乳がん / リンパ行性転移 / VEGF-C / Exosome / microRNA / hypoxia / 乳癌 / microRNA-27 / 細胞外小胞 / 低酸素 / autocrine / 高転移性乳癌 / exosome / miR27b / 乳癌細胞 / microvesicle / miRNA / 癌 / 発現抑制 / 遺伝子 / 外科 / 移植・再生医療 |
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| Outline of Final Research Achievements |
We previously reported that high expression level of VEGF-C in mouse mammary carcinoma cell (BJMC3879) caused high metastatic propensity to lymph nodes or lungs because of its ability for lymphangiogenesis. This study was aimed to demonstrate the role of the exosome mouse mammary carcinoma cell-derived, for metastasis. We hypothesized that excessive expression of miR-27b suppressed expression of VEGF-C in BJMC3879 cell was removed via secretion of exosome under the severe environment such a hypoxia condition, and BJMC3879 could proliferate by VEGF-C/VEGFR-3 system. BJMC3879 could use their exosomes containing VEGF-C due to VEGFR-3-expression on their cell membrane.
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| Academic Significance and Societal Importance of the Research Achievements |
miR-27bのexosomeによる排出を止める、またはmiR-27bを遺伝子導入すればVEGF-Cの発現が低下し、乳癌の増殖、転移をおさえることができる。女性の死亡原因の上位にある乳癌の核酸医学的治療の基礎をかためることができたと言える。
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