期刊
CELL REPORTS
卷 24, 期 7, 页码 1790-1801出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.07.043
关键词
-
类别
资金
- KAKENHI [21590445, 26430122, 16K10677]
- Japan Science and Technology Agency JST-A-STEP program [AS2621651Q]
- Japan Agency for Medical Research and Development AMED-P-CREATE [16cm0106209h0001, 17cm0106209h0002]
- Grants-in-Aid for Scientific Research [16K10677, 21590445, 26430122] Funding Source: KAKEN
Immune dysfunction is a strong factor in the resistance of cancer to treatment. Blocking immune checkpoint pathways is a promising approach to improve anti-tumor immunity, but the clinical efficacies are still limited. We previously identified follistatin-like 1 (FSTL1) as a determinant of immune dysfunction mediated by mesenchymal stromal/stem cells (MSCs) and immunoregulatory cells. Here, we demonstrate that blocking FSTL1 but not immune checkpoint pathways significantly suppresses cancer progression and metastasis in several mouse tumor models with increased MSCs. Expression of DIP2A (the receptor of FSTL1) in tumor cells is critical for FSTL1 -induced immunoresistance. FSTL1/DIP2A co-positivity in tumor tissues correlates with poor prognosis in NSCLC patients. Thus, breaking the FSTL1 -DIP2A axis may be a useful strategy for successfully inducing anti-tumor immunity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据