lncRNA SNHG16 is associated with proliferation and poor prognosis of pediatric neuroblastoma
lncRNA SNHG16 is associated with proliferation and poor prognosis of pediatric neuroblastoma
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lncRNA SNHG16与小儿神经母细胞瘤的增殖和不良预后相关
DOI：
10.3892/ijo.2019.4813
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发表时间：
2019
影响因子：
5.2
通讯作者：
Ni Xin
中科院分区：
文献类型：
--
作者：
Yu Yongbo;Chen Feng;Yang Yeran;Jin Yaqiong;Shi Jin;Han Shujing;Chu Ping;Lu Jie;Tai Jun;Wang Shengcai;Yang Wei;Wang Huanmin;Guo Yongli;Ni Xin
神经母细胞瘤(NB)是儿童最常见的颅外实体瘤之一，其分子机制复杂。越来越多的证据表明，长非编码RNA(LncRNAs)与NB的发病有关。然而，小核仁RNA宿主基因16(SNHG16)在NB中的功能目前尚不清楚。在本研究中，使用公开的数据和临床标本验证SNHG16在NB中的表达。通过集落形成、实时细胞增殖和迁移实验显示细胞的增殖和迁移状态。用流式细胞术检测SH-SY5Y细胞的细胞周期进程，并用吖啶橙/溴化乙锭染色和caspase-3/7活性测定检测细胞凋亡。为了探索SNHG16功能的潜在机制，利用一个在线数据库来寻找潜在的与SNHG16结合的RNA结合蛋白。SNHG16的表达与NB的临床分期相一致，且SNHG16的高表达与预后不良呈正相关。此外，SNHG16沉默抑制了SH-SY5Y细胞的增殖，抑制了细胞的迁移，并诱导细胞周期停滞于G0/G1期。此外，SNHG16沉默后，SH-SY5Y细胞中未检测到细胞凋亡。生物信息学分析表明，SNHG16通过转录和翻译途径调节NB细胞的增殖。这些结果提示SNHG16可能在神经母细胞瘤的发生发展中起重要作用，可能成为神经母细胞瘤治疗的潜在靶点。
Neuroblastoma (NB) is one of the most common extracranial solid tumors in children, which has complex molecular mechanisms. Increasing evidence has suggested that long noncoding RNAs (lncRNAs) account for NB pathogenesis. However, the function of small nucleolar RNA host gene 16 (SNHG16) in NB is currently unclear. In the present study, publically available data and clinical specimens were employed to verify the expression of SNHG16 in NB. Colony formation, real-time cell proliferation and migration assays were performed to demonstrate the status of cellular proliferation and migration. Flow cytometry was used to examine cell cycle progression in SH-SY5Y cells, and acridine orange/ethidium bromide staining and caspase-3/7 activity measurements were applied to study cell apoptosis. To explore the underlying mechanism of SNHG16 function, an online database was used to identify potential RNA-binding proteins that bind SNHG16. The expression of SNHG16 was revealed to be in line with the clinical staging of NB, and high SNHG16 expression was positively associated with poor clinical outcome. Furthermore, SNHG16 silencing inhibited cell proliferation, repressed migration, and induced cell cycle arrest at the G0/G1 phase in SH-SY5Y cells. Additionally, apoptosis was undetectable in SH-SY5Y cells following SNHG16 silencing. Bioinformatics analysis revealed that SNHG16 regulated cell proliferation in NB through transcriptional and translational pathways. These results suggested that SNHG16 may serve important roles in the development and progression of NB, and could represent a potential target for NB therapy.