Cd276, also known as B7-H3, is an immunoregulatory protein belonging to the B7 family. It plays a key role in cancer progression and is involved in immune checkpoint regulation. Cd276 is selectively expressed in tumor cells and immune cells within the tumor microenvironment, participating in processes such as tumor cell proliferation, metastasis, and immune evasion, and is thus a promising target for cancer therapy [1,3,4].

In mouse models, genetic ablation of Cd276 in tumor-associated macrophages (TAMs) blocked efferocytosis and enhanced the expression of major histocompatibility complex class II (MHCII) of TAMs, increasing CD4+ and cytotoxic CD8+ T cell infiltration in bladder cancer [2]. In esophageal squamous cell carcinoma (ESCC), depletion of Cd276 in a 4-nitroquinoline 1-oxide (4NQO)-induced mouse model inhibited tumorigenesis and progression. Conditional knockout of Cd276 in epithelial cells downregulated CXCL1, reducing the formation of neutrophil extracellular trap networks (NETs) via the CXCL1-CXCR2 signaling axis and augmenting natural killer (NK) cells [5].

In conclusion, Cd276 is significantly involved in tumor immune evasion, proliferation, and metastasis. Gene knockout and conditional knockout mouse models have revealed its role in bladder cancer and ESCC, highlighting its potential as a therapeutic target in these cancer types. Understanding Cd276's functions through these research models provides new insights for developing cancer immunotherapies.