| Project/Area Number |
15K14394
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Tumor diagnostics
|
|---|
| Research Institution | Tokyo Medical and Dental University |
|---|
Principal Investigator |
MIKI Yoshio 東京医科歯科大学, 難治疾患研究所, 教授 (10281594)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
中西 啓 東京医科歯科大学, 難治疾患研究所, 准教授 (50321790)
|
|---|
| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 乳がん / BRCA2 / エストロゲン / エストロゲン受容体 / エストロゲン受容体α |
|---|
| Outline of Final Research Achievements |
Mutations in the BRCA2 gene are characterized by the predisposition to familial breast and ovarian cancer. BRCA2 cell cycle-dependent expression is associated with binding of the USF, Elf1, and NF-κB transcription factors to the BRCA2 promoter. Recent studies have reported that BRCA2 expression is indirectly elevated in response to estrogen-estrogen receptor (ER) activity, such as binding to transcription factor Sp1 binding sites. In this study, mutations in each of the Sp1, NF-κB, and USF binding sites using site-directed mutagenesis were introduced into the promoter luciferase vector, and estradiol-induced BRCA2 promoter activity and BRCA2 protein level in MCF7 cells was examined. We confirmed two Sp1 sites (-50 to -55 and -69 to -75) responded to estradiol-ER complex activity. These studies aim to elucidate the mechanism underlying breast cancer development by estrogen.
|
