Neuroblastoma (NB) is a common intracranial solid tumor with high mortality. Small nucleolar RNA host gene 16 (SNHG16), one of the long noncoding RNAs (lncRNAs), has been reported to be linked to the poor prognosis of NB. However, the mechanisms of SNHG16 in regulating NB progression remain poorly understood. The expression level of SNHG16 was measured by quantitative real time polymerase chain reaction (qRT-PCR). The starBase was employed to predict the interaction of miR-128-3p and SNHG16 or HOXA7, which was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell proliferation and apoptosis were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry, respectively. Transwell assay was used to detect cell invasion or migration. The mRNA and protein levels of homeobox protein A7 (HOXA7) were determined by qRT-PCR and western blot, respectively. The levels of SNHG16 and HOXA7 were conspicuously increased in NB tissues and cells, while the expression of miR-128-3p was obviously declined, compared with corresponding normal tissues and cells. SNHG16 silencing inhibited proliferation, migration and invasion and induced apoptosis of NB cells. We identified that SNHG16 directly interacted with miR-128-3p, and miR-128-3p could target the 3'UTR of HOXA7 in NB cells. Simultaneously, miR-128-3p expression was negatively associated with SNHG16 or HOXA7. Further studies indicated that SNHG16 overexpression rescued the effects of miR-128-3p-mediated on inhibiting proliferation, migration, invasion and promoting apoptosis of NB cells. Moreover, SNHG16 could modulate HOXA7 by sponging miR-128-3p in NB cells. Besides, SNHG16 silencing suppressed tumor growth in vivo. Knockdown of SNHG16 impeded proliferation, migration, invasion and induced apoptosis through the SNHG16/miR-128-3p/HOXA7 axis in NB cells.

中文翻译：

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SNHG16沉默通过海绵miR-128-3p下调HOXA7抑制神经母细胞瘤的发展。

神经母细胞瘤（NB）是一种常见的颅内实体瘤，死亡率高。小核仁RNA宿主基因16（SNHG16），长的非编码RNA（lncRNAs）之一，据报道与NB的不良预后有关。但是，尚不清楚SNHG16调控NB进程的机制。通过定量实时聚合酶链反应（qRT-PCR）测量SNHG16的表达水平。使用starBase预测miR-128-3p与SNHG16或HOXA7的相互作用，这已通过双荧光素酶报告基因检测和RNA免疫沉淀（RIP）检测得到验证。分别通过3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化物（MTT）和流式细胞术评估细胞增殖和凋亡。Transwell测定法用于检测细胞侵袭或迁移。同源框蛋白A7（HOXA7）的mRNA和蛋白水平分别通过qRT-PCR和western blot测定。与相应的正常组织和细胞相比，NB组织和细胞中SNHG16和HOXA7的含量明显增加，而miR-128-3p的表达则明显下降。SNHG16沉默抑制NB细胞的增殖，迁移和入侵，并诱导其凋亡。我们确定SNHG16直接与miR-128-3p相互作用，而miR-128-3p可以靶向NB细胞中HOXA7的3'UTR。同时，miR-128-3p表达与SNHG16或HOXA7负相关。进一步的研究表明，SNHG16的过表达挽救了miR-128-3p介导的抑制NB细胞增殖，迁移，侵袭和促进细胞凋亡的作用。此外，SNHG16可以通过在NB细胞中海绵化miR-128-3p来调节HOXA7。此外，SNHG16沉默抑制体内肿瘤的生长。敲低SNHG16通过NBG细胞中的SNHG16 / miR-128-3p / HOXA7轴阻止增殖，迁移，侵袭并诱导凋亡。