Immunological role and underlying mechanisms of B7-H6 in tumorigenesis.

B7 homolog 6 (B7-H6) has been identified as involved in tumorigenesis. Elucidating its role and potential mechanism of action is essential for understanding tumorigenesis and the potential development of an effective clinical strategy. Abnormal overexpression of B7-H6 in various types of tumors was reported to be linked with poor prognosis. B7-H6 suppresses the initiation of the "caspase cascade" and induces anti-apoptosis by STAT3 pathway activation to provoke tumorigenesis. B7-H6 facilitates tumor proliferation and cell cycle progression by regulating apoptosis suppressors. B7-H6 induces cellular cytotoxicity, secretion of TNF-α and IFN-γ and B7-H6-specific BiTE triggers T cells to accelerate tumorigenesis. B7-H6 induces abnormal immunological progression by HER2-scFv mediated ADCC and NKp30 immune escape to promote tumorigenesis. B7-H6 promotes tumorigenesis via apoptosis inhibition, proliferation and immunological progression. B7-H6 may a valuable potential biomarker and therapeutic strategy for diagnostics, prognostics and treatment in cancer.