PDF(Pubmed)
Abstract：
B7-H3 (CD276), an immune checkpoint molecule, is overexpressed in various types of cancer and their tumor vasculature, demonstrating significant associations with adverse clinical outcomes. In addition to its well-known immune functions, B7-H3 exhibits dual co-stimulatory/co-inhibitory roles in normal physiology and the tumor microenvironment. The non-immune functions of B7-H3 in tumor cells and the tumor vasculature, including promoting tumor cell anti-apoptosis, proliferation, invasion, migration, drug resistance, radioresistance, as well as affecting cellular metabolism and angiogenesis, have increasingly gained attention from researchers. Particularly, the co-expression of B7-H3 in both tumor cells and tumor endothelial cells highlights the higher potential and clinical utility of therapeutic strategies targeting B7-H3. This review aims to summarize the recent advances in understanding the non-immune functions of B7-H3 in tumors and provide insights into therapeutic approaches targeting B7-H3, focusing on its co-expression in tumor cells and endothelial cells. The aim is to establish a theoretical foundation and practical reference for the development and optimization of B7-H3-targeted therapies.
摘要：
B7-H3(CD276),一种免疫检查点分子，在各种类型的癌症及其肿瘤脉管系统中过表达，证明与不良临床结局显著相关。除了其众所周知的免疫功能，B7-H3在正常生理学和肿瘤微环境中表现出双重共刺激/共抑制作用。B7-H3在肿瘤细胞和肿瘤脉管系统中的非免疫功能，包括促进肿瘤细胞抗凋亡，扩散,入侵,迁移,耐药性,抗辐射性，以及影响细胞代谢和血管生成，越来越受到研究者的关注。特别是,B7-H3在肿瘤细胞和肿瘤内皮细胞中的共表达凸显了靶向B7-H3的治疗策略的更高潜力和临床效用.这篇综述旨在总结B7-H3在肿瘤中的非免疫功能的最新进展，并提供针对B7-H3的治疗方法的见解，重点是其在肿瘤细胞和内皮细胞中的共表达。旨在为B7-H3靶向治疗的开发和优化建立理论基础和实践参考。
