| Project/Area Number |
22591844
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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 | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SAKURAGI Noriaki 北海道大学, 大学院・医学研究科, 教授 (70153963)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 婦人科腫瘍学 / 卵巣癌 / 抗がん剤耐性 / microRNA / 抗ガン剤耐性 / MET / MET阻害剤 / micro RNA / アポトーシス / 抗癌剤耐性 / micfroRNA / clusterin |
|---|
| Research Abstract |
We aimed to investigate the molecular mechanism of chemoresistance and to find molecular targets to overcome chemoresistance in ovarian cancer cells. We reported that clusterin, an antiapoptotic molecule, is upregulated in paclitaxel-resistant ovarian cancer cells compared to parental cells, introduction of si-RNA or antisenseoligonucleotide against clusterin sensitized paclitaxel-resistant ovarian cancer cells to paclitaxel,clusterin immunoreactivity in ovarian cancer tissues inversely correlates with response to chemotherapy and is a prognosticator for early-stage ovarian cancer. We also reported that microRNA-31 (miR-31) is down-regulated in paclitaxel-resistant ovarian cancer cells compared to parental cells, introduction of miR-31 senstized paclitaxel-rsistant ovarian cancer cells to paclitaxel, MET, a receptor tyrosine kinase, is a direct target molecule and MET can be involved in the resistant mechanisim against paclitaxel and MET inhibitor can sensitize paclitaxel-resistant ovarian cancer cells to paclitaxel.
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