| Project/Area Number |
15K20124
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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) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | Wilms' tumor 1 (WT1) / WT1 variant / 小胞体ストレス / 薬剤耐性 / 卵巣癌 / WT1 / 細胞増殖 / 腫瘍産生能 |
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| Outline of Final Research Achievements |
The Wilms’tumor 1 gene WT1 encodes a zinc transcription factor involved in cancer-related processes. WT1 is spliced alternatively at two sites: exon 5 with 17AA and the KTS site, which exists between exons 9 and 10. Splicing at these sites yields four variants (-17AA/-KTS, +17AA/-KTS, -17AA/+KTS, and +17AA/+KTS). Forced expression of WT1 -17AA/-KTS in SKOV3ip1 cells resulted in an increase in cell proliferation compared with the control. Overexpression of -17AA/-KTS resulted in a significant increase in the disseminated tumor weight, as compared with that in tumors expressing the control vector. However, there is no correlation between WT1 variants and drug sensitivity. In response to stress such as chemotherapy, cancer cell often activate the endoplasmic reticulum (ER) stress sensor, the unfolded protein response (UPR). The drug inducing UPR inhibited cell proliferation in ovarian cancer cells. Further studies are needed to clarify the relation between UPR and drug sensitivity.
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