Research progress of B7-H3 in tumor immunity
10.3760/cma.j.cn121382-20200201-00413
- VernacularTitle:B7-H3在肿瘤免疫中的研究进展
- Author:
Chuntao GAO
1
;
Tiansuo ZHAO
;
Jing CHEN
;
Jihui HAO
Author Information
1. 天津医科大学肿瘤医院胰腺肿瘤科，国家肿瘤临床医学研究中心，天津市"肿瘤防治"重点实验室，天津市恶性肿瘤临床医学研究中心 300060
- From:
International Journal of Biomedical Engineering
2020;43(4):324-329
- CountryChina
- Language:Chinese
-
Abstract:
Immunotherapy plays an important role in tumor biology research, and there has been significant progress in target therapy for cancer. B7-H3(CD276) is an immune checkpoint from the B7 family of molecules, many of whom interact with known checkpoint markers including CTLA4, PD-1, and CD28. This molecule is over-expressed in many kinds of tumors, although the receptor of B7-H3 has not been characterized. Initially, B7-H3 was thought to co-stimulate the immune response, but recent studies have shown that it has a co-inhibitory role on T-cells, contributing to cancer cell immune evasion. Therefore, its over-expression has been linked to poor prognosis in human patients and to invasive and metastatic potential of tumors in in vitro models. Moreover, recent evidence has shown that B7-H3 influences cancer progression beyond the immune regulatory roles. In this review, we aim to characterize the roles of B7-H3 in different cancers, its relationship with other immune checkpoints, and its non-immunological function in cancer progression. Targeting B7-H3 in cancer treatment can reduce cell proliferation, progression, and metastasis, which may lead to improved therapeutic options and better clinical outcomes.
