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

Analysis of immune suppressing mechanism of pancreatic cancer stroma

Research Project

Project/Area Number 17H04156
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Gastroenterology
Research InstitutionTohoku University

Principal Investigator

Shimosegawa Tooru  東北大学, 医学系研究科, 名誉教授 (90226275)

Co-Investigator(Kenkyū-buntansha) 濱田 晋  東北大学, 医学系研究科, 助教 (20451560)
正宗 淳  東北大学, 医学系研究科, 教授 (90312579)
Project Period (FY) 2017-04-01 – 2020-03-31
Project Status Completed (Fiscal Year 2019)
Budget Amount *help
¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2019: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2018: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2017: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Keywords膵癌間質 / 酸化ストレス / 膵星細胞
Outline of Final Research Achievements

We performed knockdown experiment of integrin signal regulator in pancreatic stellate cells. We also introduced Nrf2-deletion in a pancreatic cancer model mouse, and established wild-type and Nrf2-deleted cancer cells and stellate cells.
The knockdown of integrin signal regulator resulted in the attenuation of stellate cell activation. Deletion of Nrf2 in cancer cells reduced inflammation-related molecules. Deletion of Nrf2 in stellate cells attenuated cancer promoting effects.

Academic Significance and Societal Importance of the Research Achievements

本研究の実施により、膵星細胞による癌進展促進作用にインテグリンシグナルの調節因子が寄与することが明らかになった。酸化ストレス応答の中核分子、Nrf2は膵癌細胞において炎症性シグナルに関与する複数の分子の発現を制御することが判明した。膵星細胞におけるNrf2は癌促進作用に不可欠であり、酸化ストレス応答は癌細胞・間質細胞の両者で癌進展に寄与していた。以上の知見は膵癌における細胞間相互作用が局所の炎症・免疫機構に与える影響の一端を明らかにしたものであり、治療標的としてさらなる検討を要する。

Report

(4 results)
  • 2019 Annual Research Report   Final Research Report ( PDF )
  • 2018 Annual Research Report
  • 2017 Annual Research Report

URL: 

Published: 2017-04-28   Modified: 2021-02-19  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi