• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to project page

2019 Fiscal Year Final Research Report

The mechanism underlying tumor inhibition by angiogenesis and immune cell recruitment

Research Project

  • PDF
Project/Area Number 16K08481
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field General anatomy (including histology/embryology)
Research InstitutionKindai University

Principal Investigator

HAYASAKA HARUKO  近畿大学, 理工学部, 准教授 (70379246)

Project Period (FY) 2016-04-01 – 2020-03-31
Keywords血管 / 腫瘍形成
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.

Free Research Field

細胞生物学

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。

URL: 

Published: 2021-02-19  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi