A molecular mechanism that regulates extracellular matrix degradation and cell polarity in migrating cells.
Project/Area Number |
23590356
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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 |
TAKINO Takahisa 金沢大学, がん進展制御研究所, 准教授 (40322119)
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Project Period (FY) |
2011-04-28 – 2014-03-31
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Project Status |
Completed (Fiscal Year 2013)
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Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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Keywords | 細胞運動 / 浸潤 / ECM / MMP / 癌細胞 / 運動 / 細胞外マトリックス / インテグリン / 極性 / がん浸潤 / 細胞接着 / 分解 / 情報伝達 |
Research Abstract |
We have shown that membrane-type 1 matrix metalloproteinase (MT1-MMP) regulate fibronectin (FN) assembly by cleaving it, which results in promotion of cell motility and proliferation. FN matrix assembly requires the increased cytoskeletal tension generated by cadherin adhesions. In a co-culture of Rat1 fibroblasts and MT1-MMP-silenced but not control HT1080 cells, FN fibrils extended from Rat1 to cell-matrix adhesions in HT1080 cells, and N-cadherin adhesions were formed between these cells. MT1-MMP knockdown promoted FN matrix assembly and N-cadherin adhesions in HT1080 cells, which was abrogated by double knockdown with either integrin beta1 or FN. Conversely, inhibition of N-cadherin adhesions suppressed FN matrix formation in MT1-MMP-silenced cells. These data demonstrate that FN assembly initiated by MT1-MMP knockdown results in increased N-cadherin adhesions, which are prerequisite for further FN matrix formation.
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Report
(4 results)
Research Products
(31 results)
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[Journal Article] Ligand-dependent EphB1 signaling suppresses glioma invasion and correlates with patient survival2013
Author(s)
Teng L, Nakada M, Furuyama N, Sabit H, Furuta T, Hayashi Y, Takino T, Dong Y, Sato H, Sai Y, Miyamoto KI, Berens ME, Zhao SG, Hamada JI
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Journal Title
Neuro-Oncology
Volume: 15
Issue: 12
Pages: 1710-1720
DOI
Related Report
Peer Reviewed
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[Journal Article] Integrinα3 is overexpressed in glioma stem-like cells and promotes invasion2013
Author(s)
Nakada M, Nambu E, Furuyama N, Yoshida Y, Takino T, Hayashi Y, Sato H, Sai Y, Tsuji T, Miyamoto KI, Hirao A, Hamada JI
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Journal Title
Br itish J our nal of Cancer
Volume: 108
Pages: 2516-2524
Related Report
Peer Reviewed
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[Journal Article] Integrinα3 is overexpressed in glioma stem-like cells and promotes invasion2013
Author(s)
Nakada M, Nambu E, Furuyama N, Yoshida Y, Takino T, Hayashi Y, Sato H, Sai Y, Tsuji T, Miyamoto KI, Hirao A, Hamada JI
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Journal Title
Br J Cancer
Volume: 108
Issue: 12
Pages: 2516-2524
DOI
Related Report
Peer Reviewed
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[Presentation] Glycogen synthase kinase (GSK) 3βは膠芽腫の浸潤を促進する2011
Author(s)
近野祐里, 中田光俊, 廣瀬まゆみ, 北野綾子, 宮下勝吉, 藤沢弘範, 林裕, 滝野隆久, 佐藤博, 崔吉道, 宮本謙一, 川上和之, 源利成
Organizer
第70回日本癌学会学術総会
Place of Presentation
名古屋国際会議場(愛知県)
Year and Date
2011-10-03
Related Report
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