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.

中文翻译：

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B7-H6在肿瘤发生中的免疫学作用及其潜在机制。

B7同系物6（B7-H6）已被确定与肿瘤发生有关。阐明其作用和潜在的作用机制对于理解肿瘤发生和有效的临床策略的潜在发展至关重要。据报道，B7-H6在各种类型肿瘤中的异常过度表达与不良预后有关。B7-H6抑制“半胱天冬酶级联反应”的启动并通过STAT3途径激活诱导抗凋亡，从而引发肿瘤发生。B7-H6通过调节细胞凋亡抑制剂来促进肿瘤增殖和细胞周期进程。B7-H6诱导细胞毒性，TNF-α和IFN-γ的分泌，而B7-H6特异性BiTE触发T细胞加速肿瘤发生。B7-H6通过HER2-scFv介导的ADCC和NKp30免疫逃逸诱导异常的免疫学进展，从而促进肿瘤发生。B7-H6通过细胞凋亡抑制，增殖和免疫学进程促进肿瘤发生。B7-H6对于癌症的诊断，预后和治疗可能是有价值的潜在生物标志物和治疗策略。