Long non-coding RNA SNHG15 accelerates the progression of non-small cell lung cancer by absorbing miR-211-3p.

Abstract

The aim of this study was to investigate whether lncSNHG15 promoted the proliferation and migration of non-small cell lung cancer (NSCLC) cells by binding to miR-211-3p, thereby participating in the development of NSCLC. Expressions of lncSNHG15 and miR-211-3p in NSCLC tissues and para-cancerous tissues were detected by quantitative Real-Time-Polymerase Chain Reaction (qRT-PCR). LncSNHG15 and miR-211-3p expression in NSCLC cell lines were determined as well. Furthermore, cell counting kit-8 (CCK-8) and transwell assays were performed to evaluate the effects of lncSNHG15 and miR-211-3p on cell proliferation and migration, respectively. The binding relationship between miR-211-3p and ZNF217, as well as between miR-211-3p and lncSNHG15, were further verified by the Luciferase reporter gene assay. In addition, rescue experiments were performed to verify whether lncSNHG15 promoted the proliferation and migration of NSCLC cells by degrading miR-211-3p. The expression of lncSNHG15 in NSCLC tissues was significantly higher than that of para-cancerous tissues. In particular, the expression of lncSNHG15 in NSCLC patients with stage III-IV was higher than those with stage I-II. Furthermore, lncSNHG15 over-expression remarkably promoted the proliferation and migration of NSCLC cells (A549 and H358). The Luciferase reporter gene assay further indicated that lncSNHG15 could bind to miR-211-3p. Simultaneously, miR-211-3p expression in NSCLC tissues was significantly lower than that of para-cancerous tissues. The over-expression of miR-211-3p could inhibit the proliferation and migration of A549 and H358 cells. Meanwhile, the Luciferase reporter gene assay indicated that ZNF217 was the target of miR-211-3p. In addition, the over-expression of ZNF217 reversed the inhibitory effect of miR-211-3p on the proliferative and migratory potentials of A549 and H358 cells. High expression of lncSNHG15 promoted the proliferation and migration of NSCLC cells by upregulating ZNF217 by adsorbing miR-211-3p.