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Long non‐coding RNA SNHG6 promotes the growth and invasion of non‐small cell lung cancer by downregulating miR‐101‐3p

机译:长期非编码RNA SnHG6通过下调miR-101-3p来促进非小细胞肺癌的生长和侵袭

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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.? 2020 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.
机译:背景:本研究的目的是确定非小细胞肺癌(NSCLC)中长的非编码RNA小核仁RNA宿主基因6(SNHG6)的功能及其潜在机制。方法:SNHG6或MIR的关联通过TCGA数据集评估具有NSCLC专利的临床病理特征和预后的-101-3P。通过MTT和Transwell测定评估细胞增殖和侵袭,并通过生物信息分析,荧光素酶基因报告和RNA免疫沉淀测定来验证与MiR-101-3P的SNHG6特异性结合。 QRT-PCR和Western印迹用于评估SNHG6对NSCLC细胞中miR-101-3p和染色体Y的表达的影响。体内异种移植物肿瘤模型成立,观察SNHG6敲低对肿瘤生长的影响。结果:我们发现SNHG6的表达增加与病理阶段和淋巴结浸润有关,并作为患者肿瘤复发的独立预后因素。与nsclc。沉默SNHG6表达抑制细胞生长和体外体外侵袭,但SNHG6的过度表达逆转了这些效果。此外,鉴定SnHG6作为miR-101-3p的海绵,可以降低细胞增殖并衰减SnHG6诱导的Cdex表达。 miR-101-3p或高表达Cdyl的低表达与Nsclc患者的存活率不良有关。结论:我们的研究结果证明了LNCRNA SNHG6通过下调miR-101-3p的增殖和侵袭。? 2020作者。中国肺部肿瘤集团和约翰瓦里和儿子澳大利亚发表的胸癌

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