| Project/Area Number |
17K16636
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Neurosurgery
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
NAKADA Mitsutoshi 金沢大学, 医学系, 教授 (20646690)
|
|---|
| Project Period (FY) |
2017-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2018: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | EphB4 / 膠芽腫 / ephrin-B2 / invasion / グリオーマ / ephrinB2 |
|---|
| Outline of Final Research Achievements |
EphB4 was highly expressed in glioma cell lines and glioma stem cell lines. EphB4 phosphorylation by ephrin-B2 suppressed migration and invasion and downregulation of EphB4 using small interfering RNA negated the suppression of migration and invasion induced by ephrin-B2. Stimulation of glioma cells with ephrin-B2 reduced the phosphorylated Akt levels dose dependently, which was abrogated by siRNA for EphB4. EphB4-positive cells existed only at the tumor core, whereas Ephrin-B2-positive cells existed both at invasive area and the tumor core. Ligand dependent EphB4 signaling plays a role as “stay there” signaling. Extinction of its signaling promotes the release of tumor cell on its location.
|
| Academic Significance and Societal Importance of the Research Achievements |
EphB4シグナルが腫瘍中心部で腫瘍細胞の浸潤能を抑制することを明らかにした。腫瘍浸潤部ではこのシグナルから解放され、腫瘍細胞が周囲へと浸潤することを促進している可能性がある。この機構を利用し、EphB4を標的とした膠芽腫治法開発へとつながる可能性がある。
|
