Molecular mechanisms of cancer stem cells for neoplastic cellular transformation
| Project/Area Number |
26290041
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Tumor biology
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,640,000 (Direct Cost: ¥12,800,000、Indirect Cost: ¥3,840,000)
Fiscal Year 2016: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2015: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
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| Keywords | 癌 / 幹細胞 / 上皮間葉転換 |
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| Outline of Final Research Achievements |
EMT plays a fundamental role in the early stages of cancer invasion. E-cadherin is an important regulator of EMT. We identified that DYRK2 regulates E-cadherin expression. Knockdown of DYRK2 promoted EMT and cancer invasion in vitro and in vivo.
Attenuated expression of DYRK2 promotes cancer stem-like traits in vitro, tumourigenesis in vivo, and cancer stem cell population. We found that KLF4 serves as a key molecule controlling DYRK2-mediated cancer stem cell. Reduced DYRK2 expression leads to an increase of KLF4 expression, which induces cancer stem-like properties.
We also found that mTORC1 pathway is activated in DYRK2-depleted cells. The ectopic expression of DYRK2 promoted phosphorylation for the ubiquitination and degradation of mTOR.
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Report
(4 results)
Research Products
(15 results)
