Nuclear factor-κB activating protein (NKAP) is a conserved nuclear protein that acts as an oncogene in various cancers and is associated with a poor prognosis. This study aimed to investigate the role of NKAP in neuroblastoma (NB) progression and recurrence. We compared NKAP gene expression between 89 recurrence and 134 non-recurrence patients with NB by utilizing the ArrayExpress database. The relationship between NKAP expression and clinicopathological features was evaluated by correlation analysis. We knocked down NKAP expression in NB1 and SK-N-SH cells by small interfering RNA transfection to verify its role in tumor proliferation, apoptosis, and the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. NKAP gene expression in NB tissues was significantly overexpressed in the recurrence group compared with the non-recurrence group, and NKAP was enriched in the PI3K/AKT pathway. Correlation analysis revealed NKAP expression was correlated with chromosome 11q deletion in patients with NB. Knockdown of NKAP expression significantly inhibited the proliferation and promoted the apoptosis of NB1 and SK-N-SH cells. Moreover, we found that small interfering NKAP significantly reduced p-PI3K and p-AKT expression. NKAP knockdown played an oncogenic role in NB by inhibiting PI3K/AKT signaling pathway activations both in vitro and in vivo. Our research revealed that NKAP mediates NB cells by inhibited proliferation and promoted apoptosis through activating the PI3K/AKT signaling pathways, and the expression of NKAP may act as a novel biomarker for predicting recurrence and chromosome 11q deletion in patients with NB.

核因子-κB活化蛋白（NKAP）是一种保守的核蛋白，在多种癌症中均作为癌基因发挥作用，并且预后不良。这项研究旨在调查NKAP在神经母细胞瘤（NB）进展和复发中的作用。我们利用ArrayExpress数据库比较了89例复发性和134例非复发性NB患者的NKAP基因表达。通过相关分析评估了NKAP表达与临床病理特征之间的关系。我们通过小干扰RNA转染敲低了NB1和SK-N-SH细胞中的NKAP表达，以验证其在肿瘤增殖，凋亡和磷脂酰肌醇3-激酶/蛋白激酶B（PI3K / AKT）信号通路中的作用。与非复发组相比，复发组NB组织中NKAP基因表达明显过表达，NKAP在PI3K / AKT途径中富集。相关分析表明，NB患者的NKAP表达与11q染色体缺失有关。抑制NKAP表达可显着抑制NB1和SK-N-SH细胞的增殖并促进其凋亡。此外，我们发现小的干扰NKAP会显着降低p-PI3K和p-AKT表达。NKAP敲低通过抑制PI3K / AKT信号通路的激活在NB中发挥致癌作用 抑制NKAP表达可显着抑制NB1和SK-N-SH细胞的增殖并促进其凋亡。此外，我们发现小的干扰NKAP会显着降低p-PI3K和p-AKT表达。NKAP敲低通过抑制PI3K / AKT信号通路的激活在NB中发挥致癌作用 抑制NKAP表达可显着抑制NB1和SK-N-SH细胞的增殖并促进其凋亡。此外，我们发现小的干扰NKAP会显着降低p-PI3K和p-AKT表达。NKAP敲低通过抑制PI3K / AKT信号通路的激活在NB中发挥致癌作用体外 和 体内。我们的研究表明，NKAP通过激活PI3K / AKT信号通路来抑制增殖并促进凋亡，从而介导NB细胞，并且NKAP的表达可能是预测NB患者复发和11q染色体缺失的新型生物标志物。