Inhibition of Pin1 activity suppresses tumor growth in oral cancer.
Project/Area Number |
21791966
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Surgical dentistry
|
Research Institution | Tohoku University |
Principal Investigator |
MIYASHITA Hitoshi Tohoku University, 病院, 助教 (70372323)
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 臨床腫瘍学 / プロリルイソメラーゼ Pin1 / p53 / 口腔がん / 遺伝子損傷 / 応答調節因子 / 転移 / 発現抑制 / プロリルイソメラーゼPin1 |
Research Abstract |
(1) We established oral cancer cell line with Pin1 overexpression. The growth rate of this cell line was up-regulated. (2) In this cell line, Expression level of Cyclin D1 was also up-regulated. (3) We detected Pin1 protein levels with some kinds of cancer cell line including oral cancer, colon cancer, ovarian cancer and hepatocellular carcinoma. The expression level of Pin1 in HCC was lower than that of other cance. (4) No mutation was found in all of those cell line. (5) Treatment with Pin1 inhibitor increased the population of cells in S phase at 48hr. However, there was not a specific cell cycle arrest.
|
Report
(3 results)
Research Products
(23 results)