Project/Area Number |
25740024
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Risk sciences of radiation and chemicals
|
Research Institution | Kyushu University |
Principal Investigator |
LIU Xiaohui 九州大学, 理学(系)研究科(研究院), 助教 (60596849)
|
Project Period (FY) |
2013-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | ビスフェノールA / エストロゲン様作用 / 核内受容体 / 生理活性 / 乳がん細胞 / ビスフェノールA |
Outline of Final Research Achievements |
Bisphenol A (BPA) increases tumor cell proliferation in breast cancer. We discovered that BPA’s estrogen-like activity reinforced is due to the cooperative stimulative interaction between the estrogen receptors (ERs) and the estrogen-related receptors (ERRs). The aim of this study is to elucidate the molecular mechanism of this interaction in the breast cancer cell. We first analyzed the gene expression of ERs and ERRs with and without BPA administration, and it was found that ERα and either ERRα or ERRγ cooperate for stimulative activity reinforcement together with a certain participation of some coactivators. In addition, we found that BPA binds to ER, to which ERRs work cooperatively. It was also clarified that, for cooperative function between ERα and ERRs, DNA requires a specific structure of ERE element for binding of ERα. It was also revealed that ERα and ERRs function as a homodimer for activity enhancement, although their direct interaction has not been observed.
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