| Project/Area Number |
25861484
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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 | Shinshu University |
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Principal Investigator |
YAMADA Yasushi 信州大学, 医学部附属病院, 助教(特定雇用) (60646652)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 子宮内膜症性嚢胞 / ROS / CD44v / ｘCT / 酸化ストレス / lipocalin2 / 卵巣明細胞腺癌 / 酸化ストレス耐性 / 抗癌剤耐性 / グルタチオン / CD44 variant / xCT / 卵巣子宮内膜症性嚢胞 / l卵巣明細胞腺癌 / 卵巣類内膜腺癌 / 活性酸素種 |
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| Outline of Final Research Achievements |
We investigated the expression of LCN2 in ovarian carcinoma, ovarian endometriosis (OEM) and inclusion cyst (IC) by immunohistochemical staining for LCN2. LCN2 was strongly expressed in OEM, clear cell carcinoma (CCC), and endometrioid carcinoma. In contrast, the expression of LCN2 was weak or negative in IC and serous adenocarcinoma. The patients who were strongly positive for LCN2 had a significantly shorter survival. Therefore, we examined the roles of LCN2 using CCC cell lines. It was indicated that the up-regulated expression of LCN2 correlated with increases intracellular iron concentrations. However, LCN2 reduced intracellular levels of reactive oxygen species (ROS) and DNA damage. Furthermore, the expression of LCN2 suppressed oxidative stress-induced apoptosis and prolonged cell survival. It was indicated that the mechanisms was related with increasing intracellular glutathione concentration through the up-regulated expression of xCT and CD44 variant by LCN2.
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