| Project/Area Number |
16K20290
|
|---|
| 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), がん幹細胞研究部, 研究員 (40726303)
|
|---|
| Research Collaborator |
Imai Takayuki
Matsuura Kazuto
|
|---|
| Project Period (FY) |
2016-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 下咽頭癌 / CD271 / 細胞増殖 / 細胞周期 / 下咽頭がん / 癌 |
|---|
| Outline of Final Research Achievements |
We previously reported that CD271 (p75 neurotrophin receptor) is expressed in invasive front and a marker for tumor formation and is correlated with a poor prognosis in human hypopharyngeal cancer (HPC). To elucidate the role of CD271 in HPC, we established HPC cell lines and CD271-knockdown cells using siRNA. We found that CD271-knockdown completely suppressed the cells’ tumor-forming capability both in vivo and in vitro. CD271-knockdown induced cell-cycle arrest and CDKN1C expression, whereas suppressed ERK phosphorylation. In addition, either CD271 depletion diminished the in vitro migration capability. Collectively, CD271 initiates tumor formation by increasing the cell proliferation capacity through CDKN1C suppression and ERK-signaling activation, and by accelerating the migration signaling pathway in HPC.
|
| Academic Significance and Societal Importance of the Research Achievements |
本研究は、従来有望な治療標的に乏しかった下咽頭癌に焦点を当て、CD271という分子が癌の増殖・遊走能の制御に関与することを新規に見出した。さらに、申請者はCD271の下流で細胞周期制御分子であり、がん抑制因子としても知られるCDKN1Cが抑制されることを見出しており、癌の悪性化の要因の一つである可能性を示した。これらの結果は、CD271を標的とした治療の有望性を示しており、今後さらに研究を進めることで新規治療法の開発に弾みがつくと考えられる。
|
