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2016 Fiscal Year Final Research Report

Functional analysis of clock genes in regulating the microenvironment of breast cancer

Research Project

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Project/Area Number 26870028
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Human pathology
General surgery
Research InstitutionHirosaki University

Principal Investigator

Wu Yunyan  弘前大学, 医学研究科, 助教 (40636586)

Project Period (FY) 2014-04-01 – 2017-03-31
Keywords時計遺伝子 / 乳腺 / 癌微小環境 / 血管新生
Outline of Final Research Achievements

We focused on analyzing the roles of clock genes in human breast cancer. The expression of DEC2 as well as the cell viability was upregulated when exposed MCF-7 cells to hypoxia (3% O2). Hypoxia caused the phosphorylation of Akt. DEC2 functioned as a target of the PI3K/Akt pathway and regulated the expression of c-Myc and contributed to the hypoxia-induced proliferation of MCF-7 cells.
In human esophageal carcinoma cells, DEC1 and DEC2 functioned as effectors of TGF-β, an EMT (epithelial-mesenchymal transition) inducer. Additionally, DEC1 overexpression positively related to the expression of a lymphatic vessel marker podoplanin, but DEC2 exhibited an opposite effect.

Free Research Field

医歯薬学

URL: 

Published: 2018-03-22  

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