To better treat patients with non–small cell lung cancer (NSCLC), the investigations on novel molecules affecting NSCLC progression are of vital importance. Long noncoding RNAs (lncRNAs) are identified as pivotal regulators that can affect the cellular activities of carcinomas. Long intergenic non‐protein coding RNA 667 (LINC00667) is a newly found lncRNA, and its expression pattern and potent mechanisms are still obscure in NSCLC. Our study was the first to illustrate that LINC00667 was upregulated in NSCLC and LINC00667 silence refrained the proliferation, migration, and angiogenesis of NSCLC cells in vitro. In addition, vascular endothelial growth factor A (VEGFA) was modulated by LINC00667 at posttranscriptional level. Furthermore, mechanism experiments depicted that LINC00667 recruited eukaryotic translation initiation factor 4A3 (EIF4A3) to stabilize VEGFA messenger RNA. Eventually, rescue assays implied that LINC00667 modulated NSCLC progression via EIF4A3‐stabilized VEGFA. Jointly, these findings hinted that LINC00667 was a tumor promoter in NSCLC, providing guidance for the exploration on NSCLC treatment.

中文翻译：

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LINC00667通过EIF4A3稳定VEGFA促进非小细胞肺癌的增殖，迁移和病理性血管生成。

为了更好地治疗非小细胞肺癌（NSCLC）患者，对影响NSCLC进展的新型分子的研究至关重要。长的非编码RNA（lncRNA）被确定为可能影响癌症细胞活动的关键调节因子。新发现的长基因间非蛋白编码RNA 667（LINC00667）是lncRNA，其表达模式和有效机制在NSCLC中仍然不清楚。我们的研究首次证明LINC00667在NSCLC中被上调，而LINC00667沉默抑制了NSCLC细胞的体外增殖，迁移和血管生成。此外，LINC00667在转录后水平上调节了血管内皮生长因子A（VEGFA）。此外，机理实验表明，LINC00667募集了真核翻译起始因子4A3（EIF4A3）来稳定VEGFA Messenger RNA。最终，急救分析表明LINC00667通过EIF4A3稳定的VEGFA调节了NSCLC进程。这些发现共同表明，LINC00667是NSCLC中的肿瘤启动子，为探索NSCLC治疗提供了指导。