| Project/Area Number |
23592953
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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 |
Surgical dentistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
MATSUZAWA Yusuke 北海道大学, 歯学研究科(研究院), 助教 (30351620)
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| Co-Investigator(Kenkyū-buntansha) |
OGA Noritaka 北海道大学, 大学院歯学研究科, 助教 (40548202)
HIDA Kyoko 北海道大学, 大学院歯学研究科, 特任准教授 (40399952)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 腫瘍血管内皮細胞 / 活性酸素 / 染色体異常 / 抗酸化剤 / 抗酸化物質 / 口腔癌 / 腫瘍微小環境 |
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| Research Abstract |
It is known that inflammatory cells pruduce PGE-2, COX-2 in tumor stroma. Also we have found tumor endothelial cells also express these inflammatory cytokines. Thus, we hypothesized that reactive oxygen species (ROS), which is produced in inflammation, may contribute to choromosomal abnormality or genomic instability in tumor endothelial cells (TECs). Green tea cathecin, EGCG has anti-oxidant and has anti-cancer effects. We have reported that EGCG inhibited VEGF-induced cell proliferation and migration in TEC, not in NEC (Cancer Sci. 2009). In this study, we addressed whether ROS in TEC is removed by EGCG, and analyzed the effects of ROS in TEC. By ROS accumulation, TEC could survive more compared to NEC. When ROS was induced by pyocyanin, VEGF/VEGFR signal was acitivated in TEC and it was inhibited by EGCG. In addition, ROS induced aneuploidy in NEC and EGCG inhibited VEGF and aneuploidy. These results suggested that ROS induced TEC abnormality via VEGF autocrine loop.
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