Small nucleolar RNA host gene 6 (SNHG6) was a newly discovered long non-coding RNA, which was involved in the occurrence and development of a variety of cancers and was on the rise in human cancers. However, the molecular mechanism of SNHG6 in glioma required further investigation. The levels of SNHG6, microRNA-543 (miR-543) and LIM-only protein 3 (LMO3) were detected in glioma tissues and cells by quantitative real-time polymerase chain reaction. We examined cell proliferation and apoptosis rate by methylthiazolyldiphenyl-tetrazolium bromide and flow cytometry assays, respectively. Transwell assay was used to measure cell migration and invasion. The target relationships were predicted by StarBase v.2.0 and TargetScan and confirmed by dual-luciferase reporter assay. Spearman’s test was adopted for expression correlation of SNHG6, miR-543 and LMO3 in tissues. The protein expression level of LMO3 was assessed by western blot. We found that SNHG6 was obviously upregulated in glioma tissues and cells. SNHG6 knockdown significantly repressed glioma cell proliferation, migration and invasion, and induced apoptosis. Additionally, SNHG6 directly targeted miR-543 and their expression was negatively correlated in glioma tissues. And miR-543 targeted LMO3 and their expression was also inversely correlated. We found that silencing LMO3 also inhibited the progression of glioma cells. Importantly, SNHG6 could competitively sponging miR-543 thereby modulating LMO3 in glioma cells. SNHG6 served as an oncogene and played a vital role in glioma development through miR-543/LMO3 axis.

小核仁RNA宿主基因6（SNHG6）是新发现的长非编码RNA，它参与多种癌症的发生和发展，并且在人类癌症中呈上升趋势。然而，神经胶质瘤中SNHG6的分子机制需要进一步研究。通过实时定量聚合酶链反应检测神经胶质瘤组织和细胞中的SNHG6，microRNA-543（miR-543）和仅LIM蛋白3（LMO3）的水平。我们分别通过甲基噻唑基二苯基溴化四唑和流式细胞术检测了细胞增殖和凋亡率。Transwell测定法用于测量细胞迁移和侵袭。靶标关系通过StarBase v.2.0和TargetScan进行预测，并通过双荧光素酶报告基因检测法得以证实。SNHG6的表达相关性采用Spearman检验，组织中的miR-543和LMO3。通过蛋白质印迹评估了LMO3的蛋白表达水平。我们发现SNHG6在神经胶质瘤组织和细胞中明显上调。SNHG6基因敲低显着抑制神经胶质瘤细胞增殖，迁移和入侵，并诱导凋亡。此外，SNHG6直接靶向miR-543，它们的表达在神经胶质瘤组织中呈负相关。miR-543靶向LMO3，它们的表达也呈负相关。我们发现沉默的LMO3也抑制神经胶质瘤细胞的进展。重要的是，SNHG6可以竞争性地侵染miR-543，从而调节神经胶质瘤细胞中的LMO3。SNHG6作为致癌基因，通过miR-543 / LMO3轴在神经胶质瘤的发展中起着至关重要的作用。我们发现SNHG6在神经胶质瘤组织和细胞中明显上调。SNHG6基因敲低显着抑制神经胶质瘤细胞增殖，迁移和入侵，并诱导凋亡。此外，SNHG6直接靶向miR-543，它们的表达在神经胶质瘤组织中呈负相关。miR-543靶向LMO3，它们的表达也呈负相关。我们发现沉默的LMO3也抑制神经胶质瘤细胞的进展。重要的是，SNHG6可以竞争性地侵染miR-543，从而调节神经胶质瘤细胞中的LMO3。SNHG6作为致癌基因，通过miR-543 / LMO3轴在神经胶质瘤的发展中起着至关重要的作用。我们发现SNHG6在神经胶质瘤组织和细胞中明显上调。SNHG6基因敲低显着抑制神经胶质瘤细胞增殖，迁移和入侵，并诱导凋亡。此外，SNHG6直接靶向miR-543，它们的表达在神经胶质瘤组织中呈负相关。miR-543靶向LMO3，它们的表达也呈负相关。我们发现沉默的LMO3也抑制神经胶质瘤细胞的进展。重要的是，SNHG6可以竞争性地侵染miR-543，从而调节神经胶质瘤细胞中的LMO3。SNHG6作为致癌基因，通过miR-543 / LMO3轴在神经胶质瘤的发展中起着至关重要的作用。SNHG6直接靶向miR-543，它们在神经胶质瘤组织中的表达呈负相关。miR-543靶向LMO3，它们的表达也呈负相关。我们发现沉默的LMO3也抑制神经胶质瘤细胞的进展。重要的是，SNHG6可以竞争性地侵染miR-543，从而调节神经胶质瘤细胞中的LMO3。SNHG6作为致癌基因，通过miR-543 / LMO3轴在神经胶质瘤的发展中起着至关重要的作用。SNHG6直接靶向miR-543，它们在神经胶质瘤组织中的表达呈负相关。miR-543靶向LMO3，它们的表达也呈负相关。我们发现沉默的LMO3也抑制神经胶质瘤细胞的进展。重要的是，SNHG6可以竞争性地侵染miR-543，从而调节神经胶质瘤细胞中的LMO3。SNHG6作为致癌基因，通过miR-543 / LMO3轴在神经胶质瘤的发展中起着至关重要的作用。