| Project/Area Number |
19K18706
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56040:Obstetrics and gynecology-related
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| Research Institution | Keio University |
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Principal Investigator |
Iwasa Naomi 慶應義塾大学, 医学部(信濃町), 助教 (10627152)
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| Project Period (FY) |
2019-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2021: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2020: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | 卵巣癌 / 子宮内膜症 / 卵巣明細胞癌 / エクソソーム |
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| Outline of Research at the Start |
卵巣明細胞癌は子宮内膜症に関連し、化学療法に抵抗性であり進行例の予後は不良である。申請者はこれまでの研究で明細胞癌および内膜症性嚢胞内容液中のインターロイキン24（IL-24）メッセンジャーRNA（mRNA）が早期に不死化卵巣表層上皮細胞（HOSE）にとりこまれることを見出した。内膜症性嚢胞内容液中のIL24 mRNAが卵巣表層上皮細胞に取り込まれていると考えられるため、その癌化における意義を明らかにする。
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| Outline of Final Research Achievements |
DLX3 was identified as a gene whose expression was downregulated when clear cell carcinoma tumor content fluid was added to immortalized ovarian surface epithelial cell HOSE culture medium. The expression of IL-24 was markedly upregulated when the cystic content fluid of ovarian endometriosis was added to HOSE, but when DLX3 was knocked down in HOSE, the expression of IL24 was upregulated. Thus, it was possible that reduced expression of DLX3 increased IL-24 expression, but no DLX3 expression was observed in normal ovarian surface epithelium. Therefore, it is unlikely that DLX3 contributes to the carcinogenesis. Addition of IL-24 to HOSE did not alter IL6 or STAT3, suggesting that IL-24 is unlikely to be involved in carcinogenesis.
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| Academic Significance and Societal Importance of the Research Achievements |
卵巣内膜症の内容液および明細胞癌の内容液を卵巣上層上皮細胞においてIL24の発現を上昇させることを発見した。IL24の発がんへの影響は同定できず、内因性のSTING経路の活性化などをみている可能性が考えられた、
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