2018 Fiscal Year Final Research Report
Clarification of the role of CD13 combined with N-terminal fragment of fibronectin on inflammatory bone resorption.
Project/Area Number |
16K11518
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pathobiological dentistry/Dental radiology
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Research Institution | Meikai University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
関根 圭輔 横浜市立大学, 医学部, 講師 (00323569)
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Project Period (FY) |
2016-10-21 – 2019-03-31
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Keywords | 破骨細胞 / CD13 / Fibronectin / NGR配列 / がん細胞 / HT1080 |
Outline of Final Research Achievements |
We found that N-terminal peptide A of fibronectin (Patent application 2019-115222) enhances osteoclast formation via internalization of peptide A-CD13 complex into osteoclast progenitor cells and induces apoptosis of human fibrosarcoma HT1080 highly expressing CD13 via DNA binding in nuclear. Furthermore we tried to prepare R-Etodolac- or Dox-combined peptide A to examine the drug delivery activity of it. Dox-combined peptide A was accumulated in solid tumors of HT-1080 implanted-BALB/c nude mice, and inhibited the growth. Peptide A have anti-tumor activity and tumor specific drug delivery activity.
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Free Research Field |
微生物学分野
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Academic Significance and Societal Importance of the Research Achievements |
CVCTGNGRGEWKC、GNGRGEW、CNGRC (S-S環状化)のペプチドには、破骨細胞前駆細胞機能維持活性は認められなかったが、ペプチドA(特願2019-115222)にその活性が認められた。さらに、CD13高発現ヒト線維肉腫由来HT-1080細胞に対する抗がん作用も同様にペプチドAにのみその活性が認められた。このペプチドAの抗がん活性は、正常細胞である破骨細胞前駆細胞株4B12細胞とヒトGin-1細胞では認められなかった。このことは、ペプチドAが新規抗がん剤として有効である可能性が出てきたことは、学術的・社会的意義は大きいと考える。
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