The potential mechanism of neuroblastoma (NB) progression remains elusive. We intended to uncover the role and network of long noncoding RNA (lncRNA) double homeobox A pseudogene 8 (DUXAP8) in NB. Quantitative real time polymerase chain reaction (qRT-PCR) was performed to detect the levels of DUXAP8, microRNA-29 (miR-29) and nucleolar protein 4 like (NOL4L). The proliferation, colony formation, cell cycle and metastasis of NB cells were examined by (4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, plate colony formation assay, flow cytometry and transwell assays. Western blot was conducted to detect the expression of metastasis and proliferation-associated proteins and NOL4L. The target relationship was predicted by StarBase software and was confirmed by dual-luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay. Nude mice bearing tumors were used to verify the role of DUXAP8 in vivo. We found the expression of DUXAP8 was positively related to the stage of NB tumors, and it was negatively associated with the survival rate of NB patients. DUXAP8 knockdown inhibited the proliferation, colony formation, cycle and motility of NB cells. MiR-29 could interact with DUXAP8, and DUXAP8 exacerbated NB via sponging miR-29. MiR-29 could bind to NOL4L, and the influence of NOL4L intervention on the functions of NB cells could be alleviated by the transfection of miR-29 inhibitor. NOL4L was regulated by DUXAP8/miR-29 axis in NB cells. DUXAP8 knockdown blocked the progression of NB in vivo. Collectively, DUXAP8 deteriorated NB through serving as a sponge for miR-29 to up-regulate the expression of NOL4L in vitro and in vivo.

神经母细胞瘤（NB）进展的潜在机制仍然难以捉摸。我们打算揭示长非编码 RNA (lncRNA) 双同源盒 A 假基因 8 (DUXAP8) 在 NB 中的作用和网络。进行定量实时聚合酶链反应 (qRT-PCR) 以检测 DUXAP8、microRNA-29 (miR-29) 和核仁蛋白 4 样 (NOL4L) 的水平。通过(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑(MTT)测定、平板集落形成测定、流式细胞术和transwell测定检查NB细胞的增殖、集落形成、细胞周期和转移。进行蛋白质印迹以检测转移和增殖相关蛋白和NOL4L的表达。StarBase 软件预测靶标关系，并通过双荧光素酶报告基因检测和 RNA 结合蛋白免疫沉淀 (RIP) 检测确认。用荷瘤裸鼠验证DUXAP8的作用体内。我们发现DUXAP8的表达与NB肿瘤的分期呈正相关，与NB患者的生存率呈负相关。DUXAP8 敲低抑制了 NB 细胞的增殖、集落形成、周期和运动。MiR-29 可以与 DUXAP8 相互作用，DUXAP8 通过海绵 miR-29 加剧 NB。MiR-29可与NOL4L结合，转染miR-29抑制剂可减轻NOL4L干预对NB细胞功能的影响。NOL4L 在 NB 细胞中受 DUXAP8/miR-29 轴调控。DUXAP8 敲低阻止了体内NB 的进展。总的来说，DUXAP8 通过充当 miR-29 的海绵来在体外和体内上调 NOL4L 的表达，从而使 NB 恶化。