期刊
BIOCHEMICAL PHARMACOLOGY
卷 183, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2020.114298
关键词
TNBC; B7-H3; TAMs; Angiogenesis; Combination cancer therapy
资金
- National Key Research and Development Program of China [2017YFA0205400, 2017YFA0506000]
- National Natural Science Foundation of China [81673439]
- Natural Science Foundation of Jiangsu Province [BK20161391]
The study identified the correlation between B7-H3 high-expressing TAMs and TNBC progression, suggesting the potential of B7-H3 as a promising target in clinical TNBC treatment. Targeting blockade of B7-H3 improved tumor vasculature disorder and enhanced chemotherapy and PD-1 therapy efficacy.
B7-H3 is an immune checkpoint molecule from the B7 superfamily. It has been widely studied in tumor immune evasion in certain types of cancer. In our preliminary study, we found that B7-H3 is specifically enriched in tumor-associated macrophages (TAMs) in triple-negative breast cancer (TNBC) patients and strongly correlated with poor clinical prognosis. However, the role of B7-H3 in breast cancer remains elusive. Our current study aims to explore the potential of B7-H3 as a novel target in TNBC therapy. Here, we demonstrated that B7-H3 enriched on TAMs is tightly correlated with TNBC clinical progression. B7-H3(high) TAMs exhibit great pro-metastatic and immunosuppressive functions by intriguing extracellular matrix (ECM) reconstruction and tumor angiogenesis, therefore helping tumor cell dissemination and dampening T-cell infiltration in tumor microenvironment (TME). Importantly, targeting blockade of B7-H3 by anti-B7-H3 antibody improves the tumor vasculature disorder, thereby enhancing chemotherapy and PD-1 therapy efficacy. In conclusion, our study establishes the correlation between B7-H3high TAMs and TNBC progression for the first time. By exploring the possibility of targeting B7-H3 expressed in both tumor cells and TAMs, we suggest that B7-H3 could be a promising target in clinical TNBC treatment.
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