| Project/Area Number |
24890009
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Surgical dentistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
KONDOH Miyako 北海道大学, 大学病院, 医員 (10631864)
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| Project Period (FY) |
2012-08-31 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 血管内皮細胞 / 低酸素 / 活性酸素 / 染色体異常 / 細胞 / 低酸素環境 / 染色体不安定性 |
|---|
| Research Abstract |
Tumor hypoxia is important for tumor progression. TECs upregulated several genes and have highly responsiveness to growth factor and resistant to some anti-cancer drugs. Furthermore, there is chromosomal abnormality in TECs. However the mechanism of acquisition of these abnormalities in TECs remains to be unknown. In this study, we investigated the effects of hypoxia on TEC abnormalities.
Under hypoxic condition, gene expressions of HIF-1 alpha and VEGFA in human NECs (HMVEC) were upregulated. Furthermore, the aneuploidy rate of NEC increased under hypoxia. In addition, ROS was elevated in NEC by hypoxia and inhibition of ROS by EGCG inhibited hypoxia-induced aneuploidy in HMVEC. VEGFR inhibitor also inhibited aneuploidy induced by hypoxia. These results suggest that hypoxic condition in tumor microenvironment might be one of mechanisms of acquisition of chromosomal abnormality in tumor endothelial cells.
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