| Project/Area Number |
16K20063
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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 |
Orthopaedic surgery
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| Research Institution | Oita University |
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Principal Investigator |
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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 | 骨肉腫 / Heat shock protein 90 / MET / アドリアマイシン / Heat shock protein / Immunological Cell Death / ｈeat shock protein / ドキソルビシン / HSP90阻害剤 |
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| Outline of Final Research Achievements |
Recently, inhibition of heat shock protein 90 (HSP90), a type of molecular haperone, has attracted attention as an important treatment target, because HSP90 has the unction of stabilizing the structure of cancer-associated proteins. When we mprehensively analyzed the gene expression of osteosarcoma cell lines, we scertained that the expression of MET, a type of HSP90 client protein, was niversally elevated. MET is a tyrosine kinase receptor that may possibly acquire proliferation and anti-apoptotic ability through activation from the MET protein constructed by HSP90. So, in this study, we verified the changes in MET signal activity and anti-tumor effect by administering the HSP90 inhibitor 17-DMAG to osteosarcoma cells.
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