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2019 Fiscal Year Final Research Report

Elucidation of breast cancer lung metastasis by IL-17 through the modulation of stromal cells and the development of treatment model

Research Project

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Project/Area Number 17K10544
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field General surgery
Research InstitutionMie University

Principal Investigator

Saito Kanako  三重大学, 医学部附属病院, 助教 (90447871)

Co-Investigator(Kenkyū-buntansha) 加藤 琢磨  三重大学, 医学系研究科, 准教授 (60224515)
Project Period (FY) 2017-04-01 – 2020-03-31
KeywordsIL-17 / 転移 / 腫瘍関連マクロファージ / 乳癌 / 制御性T細胞 / 血管新生
Outline of Final Research Achievements

IL-17 is a proinflammatory cytokine that plays important roles in inflammation, autoimmunity and cancer. However, the role of IL-17 on tumor metastasis is not still fully understood. We previously showed that IL-17A promoted lung metastasis of mice breast cancer cell line 4T1 before the extravasation of tumor cells by using IL-17A deficient mice. In this study, we found that IL-17A contributed to the enhancement of angiogenesis, the differentiation of M2-like suppressive macrophages from monocytes, and the increase of Foxp3+Treg cells in tumor microenvironment at early stages of tumor growth, shaping in favor of promoting metastasis. The analysis of gene expression profile of IL-17-educated macrophages is ongoing. These results will allow us to establish the treatment models which targets to IL-17.

Free Research Field

腫瘍免疫学

Academic Significance and Societal Importance of the Research Achievements

転移・再発乳癌の治癒は困難であり、いずれは遠隔転移から死に至る。本研究では乳癌の転移を促進する機序の一つとして炎症性サイトカインであるIL-17に着目した。我々はIL-17欠損マウスでは著明にマウス乳癌細胞株の肺転移が抑制されることを見出だした。本研究でIL-17はマウス乳癌腫瘍組織において単球から抑制性マクロファージへの分化誘導作用、腫瘍血管の新生作用、腫瘍細胞の血中への流入促進、抑制性の腫瘍免疫環境の促進作用を有することが示唆された。さらに転移促進機序を解明することで、腫瘍環境を利用した治療開発につなげていきたい。

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Published: 2021-02-19  

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