| Project/Area Number |
17H06710
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Tumor biology
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
Terakado Yumi 金沢大学, がん進展制御研究所, 博士研究員 (00803339)
|
|---|
| Research Collaborator |
Murakami Kazuhiro
Barker Nicholas
|
|---|
| Project Period (FY) |
2017-08-25 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | 幹細胞 / 胃がん / マウスモデル / 胃癌 |
|---|
| Outline of Final Research Achievements |
We focus on a Wnt-target Leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5) gene which is epithelial stem cell marker in stomach. To elucidate the contribution of Lgr5 expression to inflammation-driven GC initiation, we crossed inflammation-driven GC a mouse model (Gan mouse) with mouse for visualization of Lgr5 expression and depletion of Lgr5 positive cells by Diphtheria toxin (DT) treatment (Lgr5-DTR-EGFP mouse). When Lgr5 positive cells were depleted by DT, polyps were suppressed in this mouse. Furthermore, when we stopped DT treatment, polyps were developed again. Those results indicate that there is a possibility that the expression of Lgr5 is important for the development of inflammation-driven GC.
|
| Academic Significance and Societal Importance of the Research Achievements |
これまでに、新規作製したマウス(Gan/ Lgr5-DTR-EGFP)において、胃粘膜腫瘍の一部の細胞で Wnt経路に重要なLgr5遺伝子が発現し、Lgr5陽性細胞を欠損させると腫瘍が退縮するという興味深い結果を得た。この結果は、胃がんの発生にWnt経路が関与するという知見とも一致し、Lgr5陽性細胞が胃がん幹細胞として機能している可能性を示唆するものである。
|
