2011 Fiscal Year Final Research Report
Invasiveness acquired during EMT
| Project/Area Number |
20247027
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | Hokkaido University (2009-2011)
Osaka Bioscience Institute (2008) |
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Principal Investigator |
SABE Hisataka 北海道大学, 大学院・医学研究科, 教授 (40187282)
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| Project Period (FY) |
2008 – 2011
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| Keywords | EMT / 浸潤 / Arf GTPases / E-cadherin / endocytosis / AMAP1 |
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| Research Abstract |
This study aims to understand precise mechanisms by which epithelial cells acquire invasiveness during their epithelial-mesenchymal transdifferentiation (EMT). Inactivation of E-cadherin and activation of some integrins are hallmark characteristics during EMT and necessary for the invasiveness. This study identified fine mechanisms as to how these cell adhesion molecules are regulated during EMT of mammary epithelial cells.
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Research Products
(47 results)
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[Journal Article] GEP100-Arf6-AMAP1-cortactin pathway frequently used in cancer invasion is activated by VEGFR2 to promote angiogenesis2011
Author(s)
Hashimoto A., Hashimoto S., Ando R., Noda K., Ogawa E., Kotani H., Hirose M., Menju T., Morishige M., Manabe T., Toda Y., Ishida S. and Sabe H.
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Journal Title
PLoS One
Volume: 6
Pages: e23359
DOI
Peer Reviewed
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[Journal Article] GEP100 links epidermal growth factor receptor signalling to Arf6 activation to induce breast cancer invasion2008
Author(s)
Morishige M., Hashimoto S., Ogawa E., Toda Y., Kotani H., Hirose M., Wei S., Hashimoto A., Yamada A., Yano H., Mazaki Y., Kodama H., Nio Y., Manabe T., Wada H., Kobayashi H. and Sabe H.
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Journal Title
Nat Cell Biol
Volume: 10
Pages: 85-92
DOI
Peer Reviewed
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