| Project/Area Number |
18K16852
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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 56050:Otorhinolaryngology-related
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2020: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 上皮間葉移行 / microRNA / 甲状腺未分化癌 |
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| Outline of Final Research Achievements |
The current study examines the role of miR-200b in mesenchymal to epithelial transition in ATC. Total RNA and miRNA isolation were performed from ATC cell lines, and ATC cell lines were transfected with miR-200b mimic. After miR-200b mimic transfection, expression levels of E-cadherin, vimentin and ZEB1 were confirmed. We evaluated miR-200b mimic and scrambled negative transfected cells for cell migration.
In ATC cell lines, mesenchymal marker ZEB1 was significantly increased and epithelial marker E-cadherin was significantly decreased. Meanwhile, mesenchymal marker vimentin was significantly higher in one ATC cell line. MiR-200b mimic transfection significantly elevated vimentin and ZEB1 expression, but E-cadherin expression remained below the measurement sensitivity. Enforced miR-200b expression slowed down cell migration. The current study suggests that miR-200b regulates mesenchymal markers vimentin and ZEB1 in ATC and promotes mesenchymal to epithelial transition.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では甲状腺未分化癌がもつ高転移能、高浸潤能についての新たな核酸治療の候補としてmicroRNA200bの可能性について検討した。
in vitroの実験ではあるが、甲状腺未分化癌細胞株にmicroRNA200bを再導入することで、甲状腺未分化癌がもつ転移能をコントロールすることができた。
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