| Project/Area Number |
13670540
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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 | Yokohama City University Hospital |
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Principal Investigator |
SATOH Shinobu Yokohama City University Hospital, University Hospital Assistant Professor, 医学部附属病院, 講師 (80244424)
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| Co-Investigator(Kenkyū-buntansha) |
SAITOH oshifumi Yokohama City University Hospital, University Hospital Associate Professor, 医学部附属病院, 助教授 (30254163)
ITO Takaaki Yokohama City University Hospital, School of Medicine Associate Professor, 医学部, 助教授 (70168392)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | glucose transporter / pancreatic cancer / gene therapy / proliferation / invasion / p21 / MAPkinase / cell cycle / 糖輸送活性 / 細胞増殖 |
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| Research Abstract |
We attempted to suppress glucose transporter 1 (GLUT1) expression by transfecting various human pancreas cancer cell line (Capan-2, PANC-1, AsPC-1, BxPC3) with cDNA for antisense GLUT1. Glucose transport was significantly decreased in cells with antisense GLUT1 compared with wild-type cells or cells with vector aione. The cell proliferation of the Capan-2 (aGLUT1) which controlled a GLUT1 expression was measured with MTT method. Compared in the wild strain (Wt), it shows about 35% of control. Glucose transport activity showed a decrease up to 24%. MAP Kinase activity with a aGLUT1 cell line revealed remarkably decrease. Suppression of GLUT1 mRNA resulted in a decreased number of cells in the S phase in the analysis of the cell cycle. This was accompanied by overexpression of p21 protein. The effect which even other human pancreas cancer cell lines, PANC-1, AsPC-1, and BxPC-3, were similar results and tend to depend on the amount of GLUT1 expression.
These results suggest that antisense GLUT1 mRNA inhibits tumor growth through a G(1) arrest and the expression of antisense GLUT1 mRNA via gene therapy can be used as a fool in the treatment of pancreas cancer.
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