2011 Fiscal Year Final Research Report
The role of TRPV2 channel trafficking in cancer cell adhesion and motility
| Project/Area Number |
21591627
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Gunma University |
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Principal Investigator |
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| Project Period (FY) |
2009 – 2011
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| Keywords | カルシウムチャネル / 癌細胞 / 細胞運動 |
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| Research Abstract |
TRPV2 channel was expressed in various cancer cells. In the present study, human fibrosarcoma cell lines was selected as a model system. Stimulation by EGF induced translocation of TRPV2 to the plasma membrane by a phosphatidylinositol (PI) 3-kinase-dependent mechanism. Moreover, an application of EGF caused a sustained increase of cytoplasmic calcium. Knock down of TRPV2 or TRP inhibitors blocked the changes in free calcium concentration. TRPV2 was localized at the filopodia or lamellipodia in the cells. TRPV2 also colocalized with focal adhesion structures, such as β-integrin, paxiliin, and vinculin. To further analyze these localization of TRPV2, vinculin conformation sensor FRET probe or vinculin tension sensor FRET probe was used. The vinculin conformation changes and calcium changes were observed around the front of the migrating cells. TRPV2 trafficking is related with the recycling of the plasma membrane.
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