| Project/Area Number |
26861427
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Otorhinolaryngology
|
|---|
| Research Institution | Miyagi Prefectural Hospital Organization Miyagi Cancer Center |
|---|
Principal Investigator |
Mochizuki Mai 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), 発がん制御研究部, 研究技師 (40726303)
|
|---|
| Research Collaborator |
Tamai Keiichi
Imai Takayuki
Sugawara Sayuri
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 下咽頭癌 / CD271 / 細胞周期 / 頭頸部癌 / 細胞増殖 / 浸潤 / がん幹細胞 |
|---|
| Outline of Final Research Achievements |
We previously reported that CD271 (p75 neurotrophin receptor) is a marker for tumor formation and correlated with a poor prognosis in human hypopharyngeal cancer. To elucidate the role of CD271 in HPC, we established HPC cell lines and CD271-knockdown cells using siRNA. We revealed that CD271-knockdown strongly suppressed the tumorigenesis and cell growth.In addition, CD271 depletion diminished the in vitro migration capability of the HPC cells. Collectively, CD271 initiates tumor formation by increasing the cell proliferation capacity and by accelerating the migration signaling pathway in HPC.
|
