The mechanism of CD9 and development of gene therapy for lung cancer
Project/Area Number |
13671417
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Thoracic surgery
|
Research Institution | KURUME 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)
|
Keywords | CD9 / 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.
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Report
(3 results)
Research Products
(4 results)