| Project/Area Number |
16H07009
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
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| Project Period (FY) |
2016-08-26 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | carbonyl reductase 1 / EMT / MET / TGF-beta / CBR1 / TGFβ / 子宮肉腫 / 間葉上皮転換 / ドラッグデリバリーシステム |
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| Outline of Final Research Achievements |
Methods: (1) We established the clone overexpressing CBR1 of ULMS cell line, SKN cells. Activities of cell proliferation, migration, and invasion were evaluated. Expressions of MET-related markers and TGFβproduction were analyzed. (2) To investigate whether suppression of TGFβ signaling induces MET, SKN cells were treated with TGFβ receptor blocker (SB431542).
Results: (1) CBR1 overexpression suppressed the activities of cell proliferation, migration, and invasion, and TGFβ production. Expressions of epithelial markers of MET were increased while mesenchymal markers were decreased by overexpression of CBR1. (2) SB431542 increased E-cadherin expression with the decrease in snail expression, indicating TGFβ signaling suppresses MET.
Conclusions: Overexpression of CBR1 induces MET by suppressing TGFβ signaling, which may be involved in the inhibition of the malignant behavior in ULMS. This study provides a novel therapeutic strategy targeting CBR1 for ULMS.
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