Long non-coding RNA SNHG6 promotes the growth and invasion of non-small cell lung cancer by downregulating miR-101-3p
Long non-coding RNA SNHG6 promotes the growth and invasion of non-small cell lung cancer by downregulating miR-101-3p
复制标题
DOI：
10.1111/1759-7714.13371
复制
发表时间：
2020-05-01
期刊：
影响因子：
2.9
通讯作者：
Zhuang, Li
中科院分区：
文献类型：
--
作者：
Li, Ke;Jiang, Yongxin;Zhuang, Li
本研究旨在探讨长链非编码RNA小核仁RNA宿主基因6 （SNHG6）在非小细胞肺癌（NSCLC）中的作用及其机制。方法采用TCGA数据集评估SNHG6或miR-101-3p与非小细胞肺癌患者临床病理特征和预后的关系。通过MTT和Transwell实验评估细胞增殖和侵袭，通过生物信息学分析、荧光素酶基因报告和RNA免疫沉淀实验验证snhg6特异性结合miR-101-3p。采用qRT-PCR和Western blot检测SNHG6对NSCLC细胞中miR-101-3p和Y样色域（CDYL）表达的影响。建立活体异种移植瘤模型，观察SNHG6基因敲低对肿瘤生长的影响。结果我们发现SNHG6表达升高与病理分期、淋巴结浸润有关，是NSCLC患者肿瘤复发的独立预后因素。沉默SNHG6表达可抑制体外和体内细胞的生长和侵袭，但过表达SNHG6可逆转这些作用。此外，SNHG6被鉴定为miR-101-3p的海绵，可以减少细胞增殖并减弱SNHG6诱导的CDYL表达。低表达miR-101-3p或高表达CDYL与NSCLC患者的低生存率相关。我们的研究结果表明，lncRNA SNHG6通过下调miR-101-3p参与NSCLC的增殖和侵袭。
Background The aim of this study was to determine the function of long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) in non-small cell lung cancer (NSCLC) and its underlying mechanisms.Methods The association of SNHG6 or miR-101-3p with clinicopathological characteristics and prognosis in patents with NSCLC was assessed by TCGA dataset. Cell proliferation and invasion were evaluated by MTT and Transwell assays and SNHG6-specific binding with miR-101-3p was verified by bioinformatic analysis, luciferase gene report and RNA immunoprecipitation assays. qRT-PCR and Western blot was used to assess the effects of SNHG6 on the expression of miR-101-3p and chromodomain Y like (CDYL) in NSCLC cells. A xenograft tumor model in vivo was established to observe the effects of SNHG6 knockdown on tumor growth.Results We found that increased expression of SNHG6 was associated with pathological stage and lymph node infiltration, and acted as an independent prognostic factor of tumor recurrence in patients with NSCLC. Silencing SNHG6 expression repressed cell growth and invasion in vitro and in vivo, but overexpression of SNHG6 reversed these effects. Furthermore, SNHG6 was identified to act as a sponge of miR-101-3p, which could reduce cell proliferation and attenuate SNHG6-induced CDYL expression. Low expression of miR-101-3p or high expression of CDYL was related to poor survival in patients with NSCLC.Conclusions Our findings demonstrated that lncRNA SNHG6 contributed to the proliferation and invasion of NSCLC by downregulating miR-101-3p.