2006 Fiscal Year Final Research Report Summary
Effect of X-ray irradiation on tumor metastasis
| Project/Area Number |
15591286
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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 |
Radiation science
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| Research Institution | Nagasaki University |
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Principal Investigator |
MATSUDA Naoki Nagasaki University, Center for Frontier Life Sciences, Professor, 先導生命科学研究支援センター, 教授 (00304973)
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| Co-Investigator(Kenkyū-buntansha) |
IHARA Makoto Nagasaki University, Graduate School of Biomedical Sciences, Assistant Professor, 大学院医歯薬学総合研究科, 助手 (60175213)
MORITA Naoko Nagasaki University, Graduate School of Biomedical Sciences, Research Technician, 大学院医歯薬学総合研究科, 技術職員 (90380972)
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| Project Period (FY) |
2003 – 2006
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| Keywords | cell mobility / metastasis / X-ray / integrin / laminin / FAK / ERK / p53 |
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| Research Abstract |
The aim of this project was to better understand the cellular and molecular mechanisms underlying enhanced tumor invasion by X-ray irradiation, especially focusing on cell mobility and intracellular signaling originated from the interaction of cell adherence molecules with extracellular matirix. The glioma cell line A172 exhibited directed migration to laminin (LM) as revealed by the migration assay which quantitate the number of migrated cells through a micropore membrane filter. Exposure of the cells to 3Gy of X ray, which decreases cell survival to approximately 70% of unirradiated, resulted in enhanced migration associated with elevated expression of integrin-β1 subunit that binds to LM. A172M cells, a p53 mutant cell line at R248W, did not show any changes in mobility and integrin-β1 expression following X-ray irradiation. Tie enhanced interaction of integrin and LM by the irradiation was confirmed by the phosphorylations of focal adhesion kinase (FAK). Furthermore, ERK1/2, a member of MAPK and one of the signaling molecules downstream of FAK, was also phosphorylated after X-ray irradiation. These findings suggests that X-ray irradiation at a sublethal dose induces tumor invasion by, at least in part, promoting the interaction of LM and integrins which leads to elevated cellular signaling. Furthermore, p53 might play some part in that signal pathways.
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Research Products
(34 results)
