The mechanism underlying tumor inhibition by angiogenesis and immune cell recruitment
| Project/Area Number |
16K08481
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
General anatomy (including histology/embryology)
|
|---|
| Research Institution | Kindai University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2016-04-01 – 2020-03-31
|
| Project Status |
Completed (Fiscal Year 2019)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | 血管 / 腫瘍形成 / 転写因子 / リンパ節 / メラノーマ / 腫瘍血管 / 抗腫瘍免疫 / メラノーマ増殖 / 免疫細胞 / 血管内皮細胞 / 癌 |
|---|
| Outline of Final Research Achievements |
Intratumoral blood vessels support cancer cell proliferation by supplying sufficient oxygen and nutrients, and provide cancer cells with a pathway for metastasis. In this study, we revealed that transcription factor Dach1 expression might promote tumor growth and angiogenesis in tumors. We found that tumor with an increased number of blood vessels grow more vigorously in the mice that constantly expressing Dach1 (Dach1-Tg) compared with wild-type. By a fow cytometric analysis using reporter mice that specifically express mTFP1 in vascular endothelial cells, we compared the percentages of endothelial cells in Dach1-Tg- and wild-type-derived tumors.
|
| Academic Significance and Societal Importance of the Research Achievements |
腫瘍内新生血管は、癌組織に酸素や栄養を供給することで癌の生存を促進する。本研究では、リンパ球動員を媒介する高内皮細胞の形成期に特異的に発現するDach1分子が、腫瘍血管形成および免疫細胞動員を介して腫瘍形成に与える意義を検討した。Dach1の発現レベルが高い腫瘍では血管形成が促進したこと、Dach1は高内皮細胞形成期に発現することから、抗腫瘍免疫に関与する免疫細胞を癌組織へ動員する血管が形成された可能性がある。本研究から、癌組織と免疫組織の血管形成において共通に作用する転写因子の存在を明らかにすることができた。
|
Report
(5 results)
Research Products
(21 results)
