| Project/Area Number |
24791680
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | Wilms' tumor 1 (WT1) / 卵巣癌 / 腫瘍産生 / VEGF / 血管新生 / WT1 isoform / 腹水 / Wilms' tumor 1 / 発がん / 薬剤耐性 |
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| Research Abstract |
In this study, we sought to investigate the effects of WT1 splice variants on tumorigenic activity and survival in an in vivo ovarian cancer model. In mice inoculated intraperitoneally with SKOV3ip1 cells expressing WT1 -17AA/-KTS, disseminated tumor weights and production of ascites were significantly increased compared with those in mice inoculated with cells expressing the control vector. The overall survival in mice with WT1 -17AA/-KTS-expressing cells was significantly shorter than that in mice with control cells. WT1 -17AA/-KTS significantly increased the expression of vascular endothelial growth factor (VEGF) and tumor microvessel density compared with the control. These results indicated that WT1 -17AA/-KTS could enhance tumorigenic activity and could decrease patient survival through up-regulation of VEGF expression in ovarian cancers. The expression of WT1 -17AA/-KTS may induce ovarian cancer cells into a more aggressive phenotype.
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