2007 Fiscal Year Final Research Report Summary
The clarification and control of the mechanism. concerning metastasis and invasion in colorectal cancer.
| Project/Area Number |
18591473
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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 |
Digestive surgery
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| Research Institution | Nagoya City University |
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Principal Investigator |
SATO Mikinori Nagoya City University, Graduate School of Medical Sciences, Assistant Professor (20305551)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEYAMA Hiromitsu Nagoya City University, Graduate School of Medical Sciences, Associate Professor (00216946)
TAKAHASHI Hiroki Nagoya City University, Graduate School of Medical Sciences, Research Associate (30381792)
YASUDA Akira Nagoya City University, Graduate School of Medical Sciences, Research Associate (90453068)
YAMAMOTO Minoru Nagoya City University, Graduate School of Medical Sciences, Research Associate (70347417)
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| Project Period (FY) |
2006 – 2007
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| Keywords | adhesive molecule / metastasis and invasion / colorectal cancer / transcrintional factor |
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| Research Abstract |
In this study, we examined the role of c- kit receptor (KIT) signal transduction on the proliferation and invasion of colorectal cancer cells. We found that c- kit was expressed in two colorectal cancer cell lines as determined by RT-PCR, Western blot and flow cytometry. In KIT-positive lines, KIT was activated by stem cell factor (SCF). SCF enhanced cellular proliferation of positive lines as demonstrated by the WST-1 proliferation assay. Furthermore, SCF enhanced the invasive ability of KIT-positive cell lines. SCF stimulation upregulated p44/42 mitogen-activated protein kinase (MAPK) and Akt as shown by Western blot. We examined the roles played by p44/42 MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt pathways in proliferation and invasion. PI3K/Akt activity strongly correlated with proliferation and invasion while p44/42 MAPK was correlated with only invasion. In conclusion, the SCF-enhanced proliferation and invasion of KIT-positive colorectal cancer cells is achieved mainly through the PI3K/Akt pathway.
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Research Products
(27 results)
