| Project/Area Number |
18591850
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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 |
Obstetrics and gynecology
|
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| Research Institution | Fujita Health University |
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Principal Investigator |
KOMIYAMA Shin-ichi Fujita Health University, School of Medicine, Associate Professor (80256312)
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| Co-Investigator(Kenkyū-buntansha) |
HASEGAWA Kiyoshi Fujita Health University, School of Medicine, Associate Professor (60208478)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,890,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | TGFβ1 / ovarian clear cell adenocarcinoma / molecular targeting therapy / anti tumor effect / RMG-1 |
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| Research Abstract |
We studied a basic research for a new molecular targeting therapy for ovarian clear cell adenocarcinoma using transforming growth factor-beta 1 (TGFβ1). Several cell lines of human ovarian clear cell adenocarcinoma (RMG-1, RMG-2, and MO were demonstrated growth inhibition, G1 arrest, and invasion inhibition by TGFBI in vitro. RMG-1 expressed p57 mRNA and PAI-1 mRNA transcribed by TGFf31, dose-dependently. On the other hand, MIVIP2 protein expression was suppressed. Then xenograft models of RMG-1 were created in SCID mice, and tumor growth was assessed from the wet weight and the BrdU uptake. In tumor-bearing mice, the tumor weight and BrdU uptake were both lower when they were treated by TGFβ1. Furthermore, TGFβ1 combined several cytotoxic drugs (paclitaxel, SN-38, and CDDP) demonstrated growth inhibition additively for RMG-1 in vitro.
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