| Project/Area Number |
11672001
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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 |
Surgical dentistry
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| Research Institution | HEALTH SCIENCES UNIVERSITY OF HOKKAIDO |
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Principal Investigator |
SHIBATA Toshiyuki HEALTH SCIENCES UNIVERSITY OF HOKKAIDO, SCHOOL OF DENTISTRY : ASSOCIATED PROFESSOR, 歯学部, 助教授 (50226172)
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| Co-Investigator(Kenkyū-buntansha) |
ARISUE Makoto HEALTH SCIENCES UNIVERSITY OF HOKKAIDO, SCHOOL OF DENTISTRY : PROFESSOR, 歯学部, 教授 (20091407)
河野 峰 北海道医療大学, 歯学部, 助手 (00285537)
NAGAYASU Hiroki HEALTH SCIENCES UNIVERSITY OF HOKKAIDO, SCHOOL OF DENTISTRY : INSTRACTOR, 歯学部, 助手 (90265075)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | HUMAN / SCC / ORAL CANCER / EGF / INVASION / MATASTASIS |
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| Research Abstract |
In order to clear the effects of Epidermal Growth Factor (EGF) on the invasion abilities of human oral squamous cell carcinoma, five cell lines were studied. EGF enhanced the random motility of all cell lines in a dose-dependent fashion and exposure to EGF let to an increased production of urokinase type plasminogen activator and matrix metalloproteniase-9 by the same cells. These results strongly suggest the EGF may promote the invasion and metastasis of human oral squamous cell carcinomas. In this project, to reveal the signal pathway, we established s-1 clone cells, which was most sensitive clone against the EGF stimulation and also we established i-1 clone cells, which was most insensitive clone. Further studies were done using s-1 clone cells. When EGF bind to the EGF receptor, tyrosine phosphorelation is firstly occurred and subsequently PKC is activated through the activation of PLCr arising from erbB homodimer and/or activation of PI3-kinase arising from erbB3 heterodimer. Furthermore, erbB homodimer activates the nPKCd through the activation of PLC and also erbB/erbB-3 heterodimer activates aPKCe through the activation of PI3K.These results suggest that inhibition of aPKCe or nPKCd can reduce the invasion and metastasis of human oral cancer cells.
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