| Project/Area Number |
16591308
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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 | Hamamatsu University School of Medicine |
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Principal Investigator |
KAMIYA Kinji Hamamatsu University School of Medicine, Medicine, Instructor, 医学部, 助手 (20324361)
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| Co-Investigator(Kenkyū-buntansha) |
KONNO Hiroyuki Hamamatsu University School of Medicine, Medicine, Professor, 医学部, 教授 (00138033)
KITAGAWA Kyoko Hamamatsu University School of Medicine, Medicine, Instructor, 医学部, 助手 (20299605)
KITAGAWA Masatoshi Hamamatsu University School of Medicine, Medicine, Professor, 医学部, 教授 (50294971)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | colon cancer / gastric cancer / Skp2 / p27 |
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| Research Abstract |
Ubiquitin-proteasome pathway is a key system that controls cellular levels of number of proteins. This pathway is responsible not only for the degradation of short-lived proteins but also tumor suppressors, transcription factors and cell cycle proteins. Recently, it has been reported that degradation of Cdk inhibitory protein p27^<Kip1> is correlated with the prognosis of colon cancer. In this study, we investigated the molecular mechanisms of down-regulation of p27^<Kip1> and acquirement of tumor malignancy in the colon cancer.
We established two cell lines, p27-hKO,p27 hetero-knockout HCT116 human colon cancer cell line and HCT-Skp2, transfected with Skp2 expression vector into HCT116 cells. We found the degradation of p27 protein in p27-hKO,HCT-Skp2 cells. Also we found that the invasive ability of p27-hKO,HCT-Skp2 cells is higher than HCT116 cells. Furthermore we applied comprehensive gene expression analysis between p27-hKO and HCT116 using microarray. As a result, function-unknown genes were overexpressed, and we demonstrated that the invasion ability of cancer cells was further increased by transfection of these genes.
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