长链非编码 RNA MIR31HG 被 SP1 激活，并通过海绵吸附 miR-214 促进 NSCLC 细胞迁移和侵袭。
Long noncoding RNA MIR31HG is activated by SP1 and promotes cell migration and invasion by sponging miR-214 in NSCLC.
机构信息
Department of Respiratory Medicine, The Second Affiliated Hospital of Nantong University, China.
Department of Respiratory Medicine, The Second Affiliated Hospital of Nantong University, China.
出版信息
Gene. 2019 Apr 15;692:223-230. doi: 10.1016/j.gene.2018.12.077. Epub 2019 Jan 17.
Long non-coding RNAs(lncRNAs) have been reported to play pivotal roles in various cancers. Recently, MIR31HG was proposed to be involved in tumor progression. However, its role in non small cell lung cancer(NSCLC) remains elusive. In this work, we found that SP1-induced MIR31HG was significantly upregulated in NSCLC tissues and cell lines. Moreover, Cox multivariate survival analysis revealed that high MIR31HG was an independent predictor of poor overall survival(OS). Functionally, knockdown of TINCR obviously suppressed NSCLC cells migration and invasion in vitro and inhibited NSCLC cells metastasis in vivo. Mechanistically, we identified MIR31HG could act as a miR-214 sponge using RNA pull down, luciferase reporter and RIP assays. Lastly, we verified that overexpression of MIR31HG effectively reverses miR-214-induced inhibition of NSCLC cells progression. Therefore, MIR31HG might serve as a promising prognostic marker and potential therapeutic target for NSCLC patients.
长链非编码 RNA（lncRNAs）已被报道在各种癌症中发挥关键作用。最近，MIR31HG 被提出参与肿瘤进展。然而，其在非小细胞肺癌（NSCLC）中的作用仍不清楚。在这项工作中，我们发现 SP1 诱导的 MIR31HG 在 NSCLC 组织和细胞系中显著上调。此外，Cox 多变量生存分析表明，高 MIR31HG 是总生存（OS）不良的独立预测因子。功能上，TINCR 的敲低明显抑制了 NSCLC 细胞在体外的迁移和侵袭，并抑制了 NSCLC 细胞在体内的转移。机制上，我们通过 RNA 下拉、荧光素酶报告基因和 RIP 测定鉴定出 MIR31HG 可以作为 miR-214 的海绵。最后，我们验证了过表达 MIR31HG 可以有效逆转 miR-214 诱导的 NSCLC 细胞进展的抑制作用。因此，MIR31HG 可能成为 NSCLC 患者有前途的预后标志物和潜在治疗靶点。
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