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Enhanced suppression of in vivo tumorigenecity of lung cancer by molecular engineered anti-angiogenic agents

Research Project

Project/Area Number 16590761
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionJUNTENDO UNIVERSITY

Principal Investigator

TAKAHASHI Kazuhisa  Juntendo University, Respiratory Medicine, Professor, 医学部, 教授 (80245711)

Co-Investigator(Kenkyū-buntansha) MIURA Kayo  Juntendo University, Respiratory Medicine, Assistant, 医学部, 助手 (70365659)
Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,100,000 (Direct Cost: ¥2,100,000)
KeywordsEndostatin / Lung cancer / Integrin receptor / Anti-tumor effect / Recombinant protein / Mice / 受容体
Research Abstract

Endostatin (ED) is a carboxyl terminal fragment of collagen XVIII with strong anti-angiogenic activity. ED receptor has been considered specific expression on endothelial cells. Recently, direct anti-tumor effect of ED in colon cancer cells has been reported. Until now, we revealed that a5 integrin is capable of being a functional ED receptor on murine lung cancer cell line, LLC cells. We demonstrated that ED-integrin interaction modulates various in vitro biological functions of LLC cells as we had revealed that immobilized ED helps in LLC cell adhesion and migration in an integrin-dependent manner. We further demonstrated that ED inhibited LLC cell proliferation and induced apoptosis. Furthermore, down regulation of a5 integrin on LLC cells using siRNA technique diminished inhibitory effect of ED on LLC cells. In addition, the binding of ED to a5 integrin on LLC cells induced phosphorylation of focal adhesion kinase (FAK). Moreover, phosphorylation of FAK in LLC cells was inhibited by anti-a5 integrin antibody.
For generation of recombinant ED protein, we have successfully purified full length ED protein using Pichia expression system and demonstrated its inhibitory effect for human umbilical vein endothelial cells (HUVEC). Subsequently, we are engineering and generating recombinant ED proteins corresponding to several ED domains

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • Research Products

    (4 results)

All 2006 2005 Other

All Journal Article (4 results)

  • [Journal Article] Endostatin gene transfer in murine lung carcinoma cells induces vascular endothelial growth factor resulting in up-regulation of in vivo tumorigenecity2006

    • Author(s)
      Cui R et al.
    • Journal Title

      Cancer Letters 232

      Pages: 262-271

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Endostatin gene transfer in Murine Lung Carcinoma Cells induces vascular endothelial growth factor resulting in up-regulation of in vivo tumorigenecity.2005

    • Author(s)
      Cui R et al.
    • Journal Title

      Cancer Letters (印刷中)

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Signal transduction-mediated by endostatin directly modulates cellular function of lung cancer cells in vitro

    • Author(s)
      Cui R et al.
    • Journal Title

      Cancer Science (印刷中)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Signal transduction-mediated by endostatin directly modulates cellular function of lung cancer cells in vitro

    • Author(s)
      Ri Cui, Kazuhisa Takahashi et al.
    • Journal Title

      Cancer Science (in press)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary

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Published: 2004-04-01   Modified: 2016-04-21  

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