| Project/Area Number |
16K09582
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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 |
Respiratory organ internal medicine
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 肺小細胞癌治療法 / 癌 |
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| Outline of Final Research Achievements |
The purpose of this study is that SMF1, an undifferentiated regulator of neural stem cells, maintains the immaturity and poorly differentiated properties of small cell lung cancer, and is to prove that it controls the malignancy of cell carcinoma.
First, we thought that cancer growth/metastasis could be suppressed by disrupting SMF1 expression, phosphorylation, and the molecular basis of its periphery. First, we were able to perform shotgun proteomics analysis for the purpose of comprehensive identification of SMF1-binding proteins in small cell lung cancer. A protein extract of a small cell lung cancer culture (H69 cells) was immunoprecipitated with anti-SMF1 antibody beads, SMF1-binding protein was eluted, and then digested with trypsin. The SMF1 binding protein was comprehensively identified by performing shotgun proteomics analysis on this using an LC-MS mass spectrometer.
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| Academic Significance and Societal Importance of the Research Achievements |
。臨床の現場において、肺小細胞癌は、特に予後が悪いことで知られており、抗癌剤を投与しても耐性の腫瘍が出現し、脳や肝臓など多臓器に転移するという問題がある。先行研究では、SMF1を欠損させると抗癌剤耐性の肺小細胞癌も死滅することから、これまで治療が難しかった肺小細胞癌、さらには悪性度の高い癌を根絶させることのできる画期的な治療法となるので、大変意義深い研究と考える。
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