| Project/Area Number |
17K16634
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Neurosurgery
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2017-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | Aquaporin1 / Glioblastoma / 脳腫瘍 / 浸潤 / 血管新生 / 解糖系 / アクアポリン1 / アクアポリン１ / 水チャネル / 浸潤能 / 脳神経疾患 / 脳腫瘍学 |
|---|
| Outline of Final Research Achievements |
The AQP1 expression has been reported to link to tumor malignancy in brain tumors. The characteristic features of AQP1-expressed GBM remain to be clarified. We observed AQP1 expression of tumor cells in the patients with GBM by an immunohistochemistry. Overexpression of AQP1 significantly accelerated glioblastoma cell migration and invasion, but not proliferation, in vitro. It is also demonstrated that the integrity of tube formation of human endothelial cells was significantly enhanced using direct co-culture system with AQP1-expressed GBM cells. Forced expressions of AQP1 significantly downregulated the THSD7A levels in GBM cells. In human specimens, AQP1 expression was negatively correlated with THSD7A expression in GBM cells. These findings suggest that AQP1 could be implicated in tumor malignancy by facilitating migration and invasion of GBM cells as well as by causing vascular deformation via downregulating anti-angiogenic THSD7A in GBM cells.
|
| Academic Significance and Societal Importance of the Research Achievements |
Glioblastomaは世界中で多くの研究がなされている現在においても非常に予後不良な脳腫瘍である。新規治療法の開発が必要不可欠であり、その腫瘍の増殖・進展に関わる分子メカニズムの解明は重要である。AQP1に関連した本研究が腫瘍の浸潤に関わるメカニズム解明の一助になったと考えられる。
|
