| Project/Area Number |
15H06770
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Tumor biology
|
|---|
| Research Institution | Kwansei Gakuin University |
|---|
Principal Investigator |
Araki Keigo 関西学院大学, 理工学部, 助教 (50756674)
|
|---|
| Research Collaborator |
KAWAUCHI KEIKO 甲南大学, フロンティアサイエンス学部, 講師
TATEISHI HISAE 甲南大学, 先端生命工学研究所, 講師
|
|---|
| Project Period (FY) |
2015-08-28 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | 癌 / 転写因子E2F3 / 発現制御機構 / 転写 / グアニン四重鎖 / グアニン四重鎖構造 / 発現制御 |
|---|
| Outline of Final Research Achievements |
E2F3 transcription factor plays a critical role in the control of cellular proliferation. E2F3 is frequently overexpressed in various types of human cancers and considered to be involved in the malignant progression of tumors, especially prostate and bladder cancers. Guanine-rich regions of DNA, which are capable of forming G-quadruplex structures, are included in coding sequence of E2F3 and we examined whether these regions participate in the regulation of E2F3 expression. We found that these guanine-rich regions contribute to suppression of E2F3 expression in normal cells and this suppression mechanism is impaired in cancer cells. These results suggest the possibility that G-quadruplex formation of E2F3 mRNA inhibits its expression in normal cells and this G-quadruplex formation is disrupted in cancer cells. In this study, we revealed a new molecular mechanism for the regulation of E2F3 expression.
|
