2013 Fiscal Year Final Research Report
Tumor suppressor FHIT regulates tumor invasion of pancreatic cancer cells via inhibiting association of Ezrin and Actin cytoskeleton
| Project/Area Number |
23592009
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Okayama University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Toshiyoshi 岡山大学, 大学院医歯薬学総合研究科, 教授 (00304303)
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| Co-Investigator(Renkei-kenkyūsha) |
KAGAWA Shunsuke 岡山大学, 病院, 講師 (00362971)
NAGASAKA Takeshi 岡山大学, 病院, 助教 (30452569)
TAZAWA Hiroshi 岡山大学, 助教 (90415513)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 遺伝子治療 / 癌 / 転移・浸潤 |
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| Research Abstract |
Ezrin is recognized as a key component in tumor metastasis and regulated by PKC. Abnormalities of tumor suppressor FHIT, whitch shares homology with PKCI (PKC-interacting protein), have been found in pancreatic cancers. In this study, we showed that FHIT overexpression in S2-VP10 pancreatic adenocarcinoma cells by transfection of Ad- FHIT suppressed migratory/invasive capacities of tumor cells. We observed that overexpression of FHIT largely reduced threonine-phosphorylated Ezrin. Furthermore, FHIT overexpression interrupted not only Ezrin and Actin cytoskeleton interaction but also Ezrin and PKC alpha interaction. We also found Fhit and PKC alpha binding in the immunoprecipitation analysis. Ectopic activation of FHIT significantly reduced the invasive potential in S2-VP10 cells. These findings suggested that overexpression of FHIT protein might regulate tumor invasion via inhibiting Ezrin and Actin cytoskeleton interaction.
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