LINC00667 promotes the proliferation, migration, and pathological angiogenesis in non-small cell lung cancer through stabilizing VEGFA by EIF4A3.

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.