The novel non‐immunological role and underlying mechanisms of B7‐H3 in tumorigenesis

B7 homolog 3 (B7-H3) has been proven to be involved in tumorigenesis. An elucidation of its role and underlying mechanisms is essential to an understanding of tumorigenesis and the development of effective clinical applications. B7-H3 is abnormally overexpressed in many types of cancer and is generally associated with a poor clinical prognosis. B7-H3 inhibits the initiation of the "caspase cascade" by the Janus kinase/signal transducers and activators of transcription pathway to resist tumor cell apoptosis. B7-H3 accelerates malignant proliferation by attacking the checkpoint mechanism of the tumor cell cycle through the phosphatidylinositol 3-kinase and protein kinase B pathway. B7-H3 reprograms the metabolism of glucose and lipids and transforms the metabolic flux of tumor cells to promote tumorigenesis. B7-H3 induces abnormal angiogenesis by recruiting vascular endothelial growth factor and matrix metalloproteinase to tumor lesions. B7-H3 strongly promotes tumorigenesis through antiapoptotic, pro-proliferation, metabolism reprogramming, and pro-angiogenesis.