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The mechanism of CD9 and development of gene therapy for lung cancer

Research Project

Project/Area Number 13671417
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Thoracic surgery
Research InstitutionKURUME UNIVERSITY

Principal Investigator

HAYASHI Akihiro  Kurume Univ., School of Medicine, Lecturer, 医学部, 講師 (70180958)

Co-Investigator(Kenkyū-buntansha) KOSAI Ken-ichiro  Gifu Univ., School of Medicine, Assistant Professor, 医学部, 助教授 (90258418)
TERAZAKI Yasuhiro  Kurume Univ., School of Medicine, Assistant, 医学部, 助手 (30279187)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥2,000,000 (Direct Cost: ¥2,000,000)
KeywordsCD9 / Cell cycle / Lung cancer / TM4SF / 遺伝子治療
Research Abstract

The cell-surface molecule CD9 were thought to play an important role in signal transduction pathways or in the regulation of cell activation, development, proliferation, and motility, although the precise biochemical functions of CD9 remain unknown.
The purpose of this study is to define the effects of CD9 expression on cell proliferation and invasion, which is an integral step in the process of tumor metastasis and invasion, using adenovirally gene transduction in lung adenocarcinoma in vitro.
The human adenocarcinoma cell line A549 was incubated with recombinant Advs, and then cells increased the expression level of CD9 in a dosage-dependent manner. Cell proliferation assay and cell cycle analysis using flow cytometric assay with propidium iodide revealed that over-expression of CD9 induced G_2/M arrest in cell cycle. The mechanism of G_2/M arrest was thought to be dephosphorylation of cdc2/cyclin B complex, using western blotting. Moreover, the over expression of CD9 suppress the phosphorylation of MAPK/ERK, which was indicated participation in MAPK signaling pathway. The analysis using boyden chamber resulted the over expression of CD9 inhibited the number of invasion cells.
In conclusion, we have demonstrated the effects of CD9 expression on cell proliferation and invasion, which is an integral step in the process of tumor metastasis and invasion, using adenovirally gene transduction in lung adenocarcinoma in vitro.

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (4 results)

All Other

All Publications (4 results)

  • [Publications] Fukunaga M et al.: "Adenoviral herpes simplex virus thymidine kinase gene therapy in an orthotopic lunq cancer model"Ann Thorac Surg. 73・6. 1740-1746 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Terazaki Y et al.: "An optimal therapeutic expression level is crucial for suicide gene therapy for hepatic metastatic cancer in mice"Hepatology. 37・1. 155-163 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Fukunaga M, Takamori S, Hayashi A, Shirouzu K, Kosai K.: "Adenoviral herpes simplex virus thymidine kinase gene therapy in an orthotopic lung cancer model"Ann Thorac Surg. 73(6). 1740-1746 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Terazaki Y, Yano S, Yuge K, Nagano S, Fukunaga M, Guo ZS, Komiya S, Shirouzu K, Kosai K.: "An optimal therapeutic expression level in crucial for suicide gene therapy for hepatic metastatic cancer in mice"Hepatology. 37(1). 155-163 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary

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Published: 2001-04-01   Modified: 2016-04-21  

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