| Project/Area Number |
23792159
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
YAMANEGI Koji 兵庫医科大学, 医学部, 講師 (00434944)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 骨肉腫、 / HDAC inhibitor、 / DNA methylation inhibitor、 / 腫瘍血管新生 / VEGI / HDAC inhibitor / 骨肉腫 / ヒストン脱アセチル化阻害剤 / VEGI (TL1A) |
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| Research Abstract |
We investigated the effects of anti-angiogenesis by valproic acid (VPA) (HDAC inhibitor) in combination with hydralazine (Hy) (DNA methylation inhibitor) on U-2 OS and SaOS-2 human osteosarcoma cells. Vascular endothelial growth inhibitor (VEGI) are potent inhibitors to suppress endothelial cell proliferation, angiogenesis, also tumor growth and neovascularization. These inhibitions are mediated by death receptor 3 (DR3) which induces apoptosis, and its function is blocked by decoy receptor 3 (DcR3). VPA increased VEGI expression and Hy increased DR3 expression. Their combination induced further increasing effect of both VEGI and DR3 without induction of DcR3 on osteosarcomas and human microvascular endothelial cells. Furthermore, VPA treated medium of osteosarcoma cells can inhibit tube formation in vitro. Thus, these results, together, suggest that VPA and Hy are considered to be one of the promising strategies in the development of novel anticancer therapy.
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