| Project/Area Number |
15K18408
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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 |
Tumor biology
|
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| Research Institution | Aichi Cancer Center Research Institute (2016)
Osaka University (2015) |
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Principal Investigator |
Mukai Satomi 愛知県がんセンター(研究所), 分子腫瘍学部, 研究員 (10706146)
|
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| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | LATS1 / EMT / Hippo pathway / ZEB1 / Lats1 / MET |
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| Outline of Final Research Achievements |
The epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) play pivotal roles in tumor metastasis. In spite of many reports on various mechanisms of EMT, the maintenance mechanism of the mesenchymal phenotypes in transited cells remains obscure.
Here, we show that LATS1, a core kinase of the Hippo pathway, maintains mesenchymal phenotypes through phosphorylation of ZEB1 S939 and suppression of E-cadherin (a marker of epithelial cells) to inhibit reversion from mesenchymal to epithelial phenotypes in the mesenchymal-like breast cancer cell line MDA-MB-231.
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