| Project/Area Number |
15590646
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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 |
Gastroenterology
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| Research Institution | Osaka University |
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Principal Investigator |
KAWANO Sunao Osaka University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (60133138)
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| Co-Investigator(Kenkyū-buntansha) |
TSUJI Shingo Osaka University, Graduate School of Medicine, Associate professor, 大学院・医学系研究科, 講師 (40301262)
TSUJII Masahiko Osaka University, Graduate School of Medicine, Instructor, 大学院・医学系研究科, 助手 (40303937)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2004: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2003: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Helicobacter pylori / Musahi-1 / Gastric cancer / CagA |
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| Research Abstract |
In the last fiscal year, we reported that a neural RNA-binding protein Musashi-1 (MSI-1) was induced in the gastric mucosa by H.pylori infection and the induction was potently mediated by CagA, a virulent factor of H.pylori In addition, we found that MSI-1 was overexpressed in some gastric cancer tissue. Here, we investigated the significance of MSI-1 expression in gastric cancer by examining the changes in a gene expression profile and phenotypes in MSI-1-overexpressed cells.
Transfecting the Msi-1 gene in AGS gastric cancer cells without MSI-1 expression by the lipofection method, we established AGS-Msi-1 cells that constitutively expressed MSI-1. RT-PCR and Western blotting revealed that anti-apoptotic molecules such as BCL-2 were remarkably induced in AGS-Msi-1 cells, compared with the wild type and mock-transfected cells. In addition, AGS-Msi-1-cells formed significantly more colonies large in size than the wild type and mock cells. in soft agar. When apoptosis was induced by serum deprivation, AGS-Msi-1 cells exhibited anti-apoptotic properties and survived at a significantly higher rate. Furthermore, NF-κB activation was suppressed in AGS-Msi-1 cells. Taken together, the present study revealed that MSI-1 expression seemed to contribute to the development of gastric cancer by exhibiting anti-apoptotic properties. The anti-apoptotic properties may be ascribed to the changes in the activation of the NF-κB pathways
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