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Development of molecular target therapy to VEGF and VEGFR against oral cancer with RNAi methods

Research Project

Project/Area Number 17592084
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Surgical dentistry
Research InstitutionHIROSHIMA UNIVERSITY

Principal Investigator

KOIZUMI Koichi  Hiroshima University, Hospital, Assistant Professor, 病院, 助手 (30335682)

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)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
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)
Keywordsoral cancer / VEGF / molecular target therapy
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

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (3 results)

All 2005

All Journal Article (3 results)

  • [Journal Article] ヒトメラノーマ細胞におけるVEGF受容体系の機能解析2005

    • Author(s)
      小泉 浩一
    • Journal Title

      口腔組織培養学会誌 14巻・1号

      Pages: 39-40

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Pole of Vascular Endothelial Growth Factor Receptor System in the motility of Human Melanoma Cell Lines2005

    • Author(s)
      Koichi Koizumi
    • Journal Title

      The Japanese Journal of Tissue Culture Society for Dental Research 14 (1)

      Pages: 39-40

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] ヒトメラノーマ細胞におけるVEGF受容体系の機能解析2005

    • Author(s)
      小泉 浩一
    • Journal Title

      口腔組織培養学会誌 14・1

      Pages: 39-40

    • Related Report
      2005 Annual Research Report

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Published: 2005-04-01   Modified: 2016-04-21  

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