| Project/Area Number |
26640109
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor therapeutics
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| Research Institution | Japanese Foundation for Cancer Research |
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Principal Investigator |
Seimiya Hiroyuki 公益財団法人がん研究会, がん化学療法センター分子生物治療研究部, 部長 (50280623)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ポリ(ADP-リボシル)化 / 細胞運動 / アクチン / がん / 浸潤 / 細胞分裂 / 転移 |
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| Outline of Final Research Achievements |
This study aims to elucidate the functional involvement of TAB182, a binding partner of tankyrase poly(ADP-ribose) polymerase, in cell motility and invasion and its molecular mechanism. We found that TAB182 negatively regulates cancer cell motility and invasion. We identified X, a regulator of actin dynamics, as a novel TAB182-binding protein. Depletion of either TAB182 or X induced phosphorylation of cofilin, a destabilizer of the actin filaments, and enhanced cell motility and invasion. These phenomena were also induced by tankyrase overexpression and inhibited by a tankyrase inhibitor. In clinical settings, TAB182 expression was reduced in the invasive areas of pancreatic cancer. These observations suggest that aberrant expression of TAB182 may facilitate cancer cell invasion.
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