Development of molecular target therapy to VEGF and VEGFR against oral cancer with RNAi methods
| Project/Area Number |
17592084
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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 |
Surgical dentistry
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
KOIZUMI Koichi Hiroshima University, Hospital, Assistant Professor, 病院, 助手 (30335682)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMOTO Tetsuji Hiroshima University, Graduate School of Biomedical Sciences, Professor, 大学院医歯薬学総合研究科, 教授 (00169153)
HAYASHIDO Yasutaka Hiroshima University, Hospital, Assistant Professor, 病院・講師 (70243251)
YOSHIOKA Yukio Hiroshima University, Graduate School of Biomedical Sciences, Assistant, 大学院医歯薬学総合研究科, 助手 (20335665)
KOBAYASHI Masashi Hiroshima University, Graduate School of Biomedical Sciences, Assistant, 大学院医歯薬学総合研究科, 助手 (30346506)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2005: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | oral cancer / VEGF / molecular target therapy |
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| Research Abstract |
Cell migration plays a significant role in cancer invasion and metastasis. Our previous studies have shown vascular endothelial growth factor ( VEGF) and VEGF receptor 1 ( Flt-1 ) express in oral squamous cell carcinoma ( SCC ) cells. These finding suggests VEGF-VEGFR system might regulate in autocrine manner as well as angiogenesis in paracrine manner.
In this study, we examined the expression of VEGF and VEGFR in melanoma cells. The participation of VEGF and VEGFR in invasion and metastasis of melanoma cells was also investigated.
VEGF-induced proliferation of melanoma cells were suppressed by VEGFR-1 antisense oligo, but not by VEGFR-2 antisense oligo.
Checkerbord analysis showed that VEGF induced Chemotaxitic and Chemokinetic migration in melanoma cells. The VEGF-induced migration was inhibited by VEGFR tyrosine kinase inhibitor. The migration was suppressed by VEGFR-1 antisense oligo, but not by VEGFR-2 antisense oligo.
VEGF induced phosphorilation of Akt. PI3 kinase inhibitor block the VEGF-induced phosphorilation of PI3/Akt kinase cascade, and suppressed VEGF-induced motility of melanoma cells. These findings suggest that migration of melanoma cells is regulated with VEGF-induced activation of PI3/Akt kinase cascade
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Report
(3 results)
Research Products
(3 results)
