2016 Fiscal Year Final Research Report
Functional analysis of clock genes in regulating the microenvironment of breast cancer
Project/Area Number |
26870028
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Human pathology
General surgery
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Research Institution | Hirosaki 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.
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Free Research Field |
医歯薬学
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