Growth suppression of human breast cancer, based on the clock gene function

2015 Fiscal Year Final Research Report

• Project/Area Number: 25861148
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: General surgery
• Research Institution: Hirosaki University
• Principal Investigator: Morohashi Satoko 弘前大学, 医学(系)研究科(研究院), 助教 (90569592)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 乳癌 / 時計遺伝子 / 治療

Outline of Final Research Achievements

The purpase of the staging is growth suppression of human breast cancer, based on the clock gene function.
The expression of c-Myc was upregulated by exposure to hypoxia and by the overexpression of DEC2. In conclusion, DEC2 participates in hypoxia-induced cell proliferation by functioning as a target gene of the PI3K/Akt signaling pathway and regulating the expression of c-Myc in human breast cancer cell line MCF-7. We also demonstrated that DEC1 overexpression promoted cleaved PARP expression, whereas DEC2 overexpression had no effects on the amount of cleaved PARP in TE 10 cells. These results suggested that DEC1 has pro-apoptotic effects on human esophageal cancer TE 10 cells of well-differentiated type.

Free Research Field

乳腺外科病理学