Abstract

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.

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