Analysis of mechanism of serine protease activation by membrane-type matrix metalloproteinase
Project/Area Number |
25460382
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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 |
Pathological medical chemistry
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Research Institution | Kanazawa University |
Principal Investigator |
Sato Hiroshi 金沢大学, がん進展制御研究所, 教授 (00115239)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | がん転移 / マトリックスメタロプロテアーゼ / MT1-MMP / HAI-1 / セリンプロテアーゼ / MMP-9 / マトリプターゼ |
Outline of Final Research Achievements |
Membrane-Type Matrix Metalloproteinase (MT1-MMP) was shown to cleave and inactivate membrane-type serine protease inhibitor HAI-1(Hepatocyte Growth Factor Inhibitor-1), which subsequently induced activation of matriptase. Activated matriptase induced further activation of serine protease cascade, which was named “Protease Storm”. Protease storm caused Epithelial-Mesenchymal Transition (EMT) in cancer cells. These results indicate that MT1-MMP contributes to malignant transformation of cancer cells by triggering protease activation cascade.
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Report
(4 results)
Research Products
(24 results)
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[Journal Article] Suppressing TGFβ signaling in regenerating epithelia in an inflammatory microenvironment is sufficient to cause invasive intestinal cancer.2015
Author(s)
Oshima H, Nakayama M, Han TS, Naoi K, Ju X, Maeda Y, Robine S, Tsuchiya K, Sato T, Sato H, Taketo MM, Oshima M.
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Journal Title
Cancer Res.
Volume: 75
Issue: 4
Pages: 766-776
DOI
NAID
Related Report
Peer Reviewed / Open Access
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[Journal Article] Glycogen synthase kinase 3β sustains invasion of glioblastoma via the focal adhesion kinase, Rac1 and c-Jun N-terminal kinase-mediated pathway.2015
Author(s)
Chikano Y, Domoto T, Furuta T, Sabit H, Kitano-Tamura A, Ilya V. Pyko, Takino T, Sai Y, Hayashi Y, Sato H, Miyamoto K, Nakada M, MinamotoT.
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Journal Title
Molecular Cancer Therapeutics
Volume: 14
Issue: 2
Pages: 564-574
DOI
Related Report
Peer Reviewed / Open Access
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