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2016 Fiscal Year Final Research Report

Molecular mechanisms of cancer stem cells for neoplastic cellular transformation

Research Project

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Project/Area Number 26290041
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypePartial Multi-year Fund
Section一般
Research Field Tumor biology
Research InstitutionJikei University School of Medicine

Principal Investigator

YOSHIDA KIYOTSUGU  東京慈恵会医科大学, 医学部, 教授 (70345312)

Project Period (FY) 2014-04-01 – 2017-03-31
Keywords癌 / 幹細胞 / 上皮間葉転換
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.

Free Research Field

分子腫瘍学

URL: 

Published: 2018-03-22  

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