B7 family members act as co-stimulatory or co-inhibitory molecules in the adaptive immune system. Thisstudy aimed to investigate the dysregulation, prognostic value and regulatory network of B7 family members in non-small cell lung cancer (NSCLC). Data for lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) patients were extracted from public databases. Patient prognosis was determined by Kaplan–Meier analysis. The downstream signaling pathways of B7 family were identified via GO and KEGG analysis. The key B7 related genes were selected by network, correlation and functional annotation analysis. Most B7 family members were dysregulated in LUAD and LUSC. The expression of B7-1/2/H3 and B7-H5 were significantly associated with overall survival in LUAD and LUSC, respectively. The major pathway affected by B7 family was the EGFR tyrosine kinase inhibitor resistance and ErbB signaling pathway. MAPK1, MAPK3 and MAP2K1 were pivotal B7 related genes in both LUAD and LUSC. This study reveals an overall dysregulation of B7 family members in NSCLC and highlights the potential of combination use of tyrosine kinase inhibitors or MEK/ERK inhibitors with B7 member blockade for NSCLC treatment.

B7 家族成员在适应性免疫系统中充当共刺激或共抑制分子。本研究旨在调查 B7 家族成员在非小细胞肺癌 (NSCLC) 中的失调、预后价值和调控网络。从公共数据库中提取肺腺癌 (LUAD) 和肺鳞状细胞癌 (LUSC) 患者的数据。患者预后由 Kaplan-Meier 分析确定。通过 GO 和 KEGG 分析确定了 B7 家族的下游信号通路。通过网络、相关性和功能注释分析选择关键的B7相关基因。大多数 B7 家族成员在 LUAD 和 LUSC 中失调。B7-1/2/H3 和 B7-H5 的表达分别与 LUAD 和 LUSC 中的总生存显着相关。B7家族影响的主要通路是EGFR酪氨酸激酶抑制剂耐药和ErbB信号通路。MAPK1、MAPK3 和 MAP2K1 是 LUAD 和 LUSC 中的关键 B7 相关基因。这项研究揭示了 NSCLC 中 B7 家族成员的整体失调，并强调了联合使用酪氨酸激酶抑制剂或 MEK/ERK 抑制剂与 B7 成员阻断剂治疗 NSCLC 的潜力。