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2015 Fiscal Year Final Research Report

The elucidation of the mechanism by which DYRK2 expression is regulated

Research Project

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Project/Area Number 26861056
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field General surgery
Research InstitutionJikei University School of Medicine

Principal Investigator

Mimoto Rei  東京慈恵会医科大学, 医学部, 助教 (70710333)

Project Period (FY) 2014-04-01 – 2016-03-31
Keywords乳癌 / DYRK2
Outline of Final Research Achievements

Our recent study revealed that DYRK2 has a tumor-suppressive function through c-Myc, c-Jun, and Snail expression and phosphorylation of p53. DYRK2 expression is decreased in advanced breast cancer and serous ovarian cancer. Diminished expression of DYRK2 confers drug-resistance to cytotoxic chemotherapy and poor prognosis in these cancers. However, the therapeutic strategy has not been established for breast cancer patients with low DYRK2 expression. Through microarray analysis, mTORC1 pathway was detected as the activated pathway in DYRK2 depleted cells. mTOR inhibitor, everolimus treatment was associated with a significant inhibition of tumor growth compared to vehicle in vitro and in vivo.

Free Research Field

腫瘍学

URL: 

Published: 2017-05-10  

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