2012 Fiscal Year Final Research Report
Analysis of molecular mechanisms of the acquisition of tumor invasiveness
| Project/Area Number |
21370092
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 |
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Principal Investigator |
HASHIMOTO Sigeru 北海道大学, 大学院・医学研究科, 准教授 (50311303)
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| Project Period (FY) |
2009 – 2012
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| Keywords | 低酸素 / 細胞浸潤 / 癌転移 / EMT / Arf6 / AMAP1 / GEP100 |
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| Research Abstract |
We have previously shown that the GEP100-Arf6-AMAP1 pathway, activated by receptor tyrosine kinases, is involved in the acquisition of breast cancer invasiveness. Our analyses demonstrate that the activation of GEP100-Arf6-AMAP1 pathway via the c-Met/HGFR signaling is essential for the acquisition of the invasiveness of some breast cancer cells during hypoxia- or TGFss1-induced EMT. Moreover, we found that the expression of some molecules within the GEP100-Arf6-AMAP1 pathway are regulated by hypoxia-inducible factor (HIF) or EZH2, which have shown to be involved in the initiation and maintenance of the stemness in hypoxia.
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[Journal Article] GEP100-Arf6-AMAP1-cortactin pathwayfrequently used in cancer invasion isactivated 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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