| Project/Area Number |
25860092
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Drug development chemistry
|
|---|
| Research Institution | Tokyo University of Pharmacy and Life Science |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
HAMADA Keisuke
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | リードスルー / 細胞増殖抑制 / Calu-6 / calu-6 |
|---|
| Outline of Final Research Achievements |
In this research, TCP-169, which is a synthetic derivative based on (+)-negamycin, a dipeptidic antibiotic, significantly suppressed the proliferation of Calu-6 cells caused by nonsense mutation of TP53. This activity based on readthrough of nonsense mutation was significantly enhanced by the co-treatment of nutlin-3 or brefeldin A, which are a MDM-2 inhibitor or an intracellular protein transport inhibitor, respectively. Additionally, p53 protein re-expression in TCP-169-treated Calu-6 cell (p53 null) was confirmed by western blotting. On the other hand, this study suggested that TCP-169 might possess another function against cell proliferation in the cell except for accelerating re-production of p53 protein. Therefore, elucidation of the detailed anti-proliferative mechanism of TCP-169 is expected in the future work.
|
