| Project/Area Number |
09672062
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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)
NAGAYASU Hiroki HEALTH SCIENCES UNIVERSITY OF HOKKAIDO SCHOOL OF DENTISTRY : INSTRACTOR, 歯学部, 助手 (90265075)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | HUMAN / SCC / ORAL CANCER / EGF / INVASION / MATASTASIS / INVASIN |
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| Research Abstract |
1) Effect of EGF in paracrine manner
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.
2) EFFECT OF EGE IN AUTOCRINE MANNER
Cell lines, which produced EGF, was found out in these cell lines. In these cells, EGF producedby tumor cells can stimulate the random motility itself through the EGF receptor.
3) ESTABLISHMENT OF EGF SENSITIVE CLONE
To reveal the signal pathway, we established s-1 clone cells, which was most sensitive clone against the EGE stimulation and also we established i-1 clone cells, which was most insensitive clone.
4) ANALYSIS OF SIGNAL TRANSDUCTION OF EGF-INDUCED MOTILITY
When EGE 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 br activation of P13-kinase arising from erbB3 heterodimer.
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