Department of Respiratory and Critical Medicine, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Eur Rev Med Pharmacol Sci. 2019 Feb;23(4):1536-1544. doi: 10.26355/eurrev_201902_17112.
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.
本研究旨在探讨长链非编码 RNA SNHG15（lncSNHG15）是否通过与 miR-211-3p 结合，从而参与非小细胞肺癌（NSCLC）的发展，进而促进 NSCLC 细胞的增殖和迁移。
采用实时荧光定量聚合酶链反应（qRT-PCR）检测 NSCLC 组织和癌旁组织中 lncSNHG15 和 miR-211-3p 的表达。还测定了 NSCLC 细胞系中 lncSNHG15 和 miR-211-3p 的表达。此外，通过细胞计数试剂盒-8（CCK-8）和 Transwell 测定分别评估 lncSNHG15 和 miR-211-3p 对细胞增殖和迁移的影响。通过荧光素酶报告基因测定进一步验证了 miR-211-3p 与 ZNF217 以及 miR-211-3p 与 lncSNHG15 之间的结合关系。此外，通过进行挽救实验来验证 lncSNHG15 是否通过降解 miR-211-3p 促进 NSCLC 细胞的增殖和迁移。
lncSNHG15 在 NSCLC 组织中的表达明显高于癌旁组织。特别是，III-IV 期 NSCLC 患者的 lncSNHG15 表达高于 I-II 期患者。此外，lncSNHG15 的过表达显著促进了 NSCLC 细胞（A549 和 H358）的增殖和迁移。荧光素酶报告基因测定进一步表明 lncSNHG15 可以与 miR-211-3p 结合。同时，miR-211-3p 在 NSCLC 组织中的表达明显低于癌旁组织。miR-211-3p 的过表达可抑制 A549 和 H358 细胞的增殖和迁移。同时，荧光素酶报告基因测定表明 ZNF217 是 miR-211-3p 的靶标。此外，ZNF217 的过表达逆转了 miR-211-3p 对 A549 和 H358 细胞增殖和迁移潜能的抑制作用。
高表达的 lncSNHG15 通过吸附 miR-211-3p 上调 ZNF217 促进 NSCLC 细胞的增殖和迁移。
