B7-H1 and B7-H3 are independent predictors of poor prognosis in patients with non-small cell lung cancer.
B7-H1 and B7-H3 are independent predictors of poor prognosis in patients with non-small cell lung cancer.
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B7-H1和B7-H3是非小细胞肺癌患者预后不良的独立预测因子
DOI：
10.18632/oncotarget.3097
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发表时间：
2015-02-20
期刊：
影响因子：
--
通讯作者：
Tao M
中科院分区：
文献类型：
--
作者：
Mao Y;Li W;Chen K;Xie Y;Liu Q;Yao M;Duan W;Zhou X;Liang R;Tao M
B7-H1和B7-H3是B7家族的两个成员，被认为调节T细胞活化，在人非小细胞肺癌（NSCLC）中表达。然而，其预后意义知之甚少。在本研究中，我们报告了B7-H1和B7-H3分别在96/128（72.7%）和89/128（69.5%）样本中表达。NSCLC组织中B7-H1、B7-H3的表达及浸润的T细胞胞内抗原1+、γ-干扰素+细胞数均显著高于癌旁组织（p<0.01）。B7-H1和B7-H3高表达与淋巴结转移和TNM分期有关（p<0.05）。在多变量考克斯比例风险回归模型中，性别、TNM分期、B7-H1、B7-H3和T细胞胞内抗原-1表达在校正其他预后因素后仍是显著的预后因素。体外研究表明，当抗CD 3和抗CD 28单克隆抗体刺激时，敲低肿瘤细胞上的B7-H3增强T细胞生长和干扰素-γ分泌。干扰素-γ可降低CXCR 4在癌细胞上的表达，并抑制CXCL 12诱导的细胞迁移。B7-H1和B7-H3是NSCLC患者生存率较差的独立预测因子。干扰这些负调控分子的信号通路可能成为治疗NSCLC的新策略。
B7-H1 and B7-H3, two members of the B7 family that are thought to regulate T-cell activation, are expressed in human non-small cell lung cancer (NSCLC). However, their prognostic significance is poorly understood. In the present study we reported that B7-H1 and B7-H3 were expressed in 96/128 (72.7%) and 89/128 (69.5%) samples, respectively. B7-H1 and B7-H3 expression and the number of infiltrating T-cell intracellular antigen-1+ and interferon-γ+ cells in NSCLC tissues were significantly higher than those in the adjacent tissues (p<0.01). High B7-H1 or B7-H3 expression was associated with lymph node metastasis and TNM stage (p<0.05, respectively). Sex, TNM stage, B7-H1, B7-H3, and T-cell intracellular antigen-1 expression remained significant prognostic factors after adjusting for other prognostic factors in a multivariate Cox proportional hazards regression model. In vitro studies revealed that knockdown of B7-H3 on tumor cells enhanced T-cell growth and interferon-γ secretion when stimulated by anti-CD3 and anti-CD28 monoclonal antibodies. Interferon-γ reduced CXCR4 expression on cancer cells and inhibited the CXCL12-induced cell migration. B7-H1 and B7-H3 are independent predictors of poorer survival in patients with NSCLC. Interference of the signal pathways of these negative regulatory molecules might be a new strategy for treating NSCLC.
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