| Project/Area Number |
23592432
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
UTSUNOMIYA Hiroki 東北大学, 医学(系)研究科(研究院), 准教授 (10359507)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Fumihiko 東北大学, 大学院医学系研究科, 助教 (20400343)
鍋島 寛志 東北大学, 大学病院, 助教 (90547415)
|
|---|
| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| Keywords | 子宮内膜癌 / レチノイン酸 / エストロゲン受容体 / レチノイン酸受容体 / SMAD3 / クロマチン免疫沈降クローニング / 培養細胞 |
|---|
| Research Abstract |
We focused on the novel target areas of mutual transcription factor for RARa and ERa. And then, we tried to detect the genes and its novel molecular mechanism.
At first, we revealed the opposite functions between RARa and ERa. And then, we studied the target binding area of RARa and ERa using ChIP cloning technique, and found the promoter lesions of SMAD3. In addition, SMAD3 was significantly decreased after knock-down for RARa and addition of AM580 treatment compared with the control data.
Our findings suggested that SMAD3 genes, which were deeply correlated with AM580 treatment, might play important biological roles in endometrial cancer.
|
