Abstract
BackgroundTo explore the role of non‐coding RNA activated by DNA damage (NORAD), a long non‐coding ribonucleic acid (lncRNA), in non‐small cell lung cancer (NSCLC) and its possible mechanism.MethodsQuantitative real‐time polymerase chain reaction was adopted for the detection of the expression levels of NORAD, micro RNA (miR)‐656‐3p, and AKT serine/threonine kinase 1 (AKT1). The effects of NORAD, miR‐656‐3p, and AKT1 on cell proliferation and migration were examined through the Cell Counting Kit‐8 (CCK‐8) and Transwell assay. Subsequently, the binding relationships between miR‐656‐3p and AKT1 and between miR‐656‐3p and NORAD were verified by dual‐luciferase reporter gene assay. Finally, the potential mechanisms of action of NORAD and miR‐656‐3p were explored through the torsion experiment.ResultsThe lncRNA NORAD expression level in NSCLC patients was notably higher than that in people in control group, that in patients with metastasis was higher than that in patients without metastasis, and that in patients with NSCLC in stage III‐IV was significantly higher than that in patients with NSCLC in stage I‐II. Elevation of NORAD stimulated the proliferation and migration of NSCLC A549/H460 cells. According to the reporter gene assay, NORAD could bind to miR‐656‐3p. Besides, miR‐656‐3p was significantly under‐expressed in cancer tissues of patients with NSCLC, and overexpression of miR‐656‐3p could block the proliferation and migration of A549/H460 cells and reversed promotion on cell proliferation and migration by NORAD. Furthermore, the reporter gene assay revealed that the overexpression of AKT1, a miR‐656‐3p target gene, could reverse miR‐656‐3p's inhibitory effect on the proliferation and migration of A549/H460 cells.ConclusionLncRNA NORAD is capable of promoting the proliferation and migration of NSCLC cells, and its mechanism may be that it increases the AKT1 expression by adsorbing miR‐656‐3p.
Highlights
Lung cancer is a malignant tumor, whose incidence and mortality rates were the highest worldwide, which seriously threatens human life and health (Jemal, Siegel, Xu, & Ward, 2010; McGuire, 2016; Wei, Tian, Song, Wu, & Liu, 2018)
Lung cancer can be divided into two types, namely, small cell lung cancer and non‐small cell lung cancer (NSCLC), and the incidence rate of the latter takes up 80%–90% of the total of lung cancer (Stewart et al, 2014)
The expression level of long non‐coding ribonucleic acid (lncRNA) non‐coding RNA activated by DNA damage (NORAD) in lung cancer tissues and corresponding cancer‐adjacent tissues was measured, and it was found that NORAD was obviously highly expressed in lung cancer tissues (Figure 1a)
Summary
Lung cancer is a malignant tumor, whose incidence and mortality rates were the highest worldwide, which seriously threatens human life and health (Jemal, Siegel, Xu, & Ward, 2010; McGuire, 2016; Wei, Tian, Song, Wu, & Liu, 2018). More and more in‐depth studies have verified that lncRNAs regulate the gene expression at both transcriptional and post‐transcriptional levels as well as the epigenetic level, so as to exert crucial effects on tumor initiation, progression, and metastasis, proving that they are potential prognostic markers and therapeutic targets for tumors (Hennessy, 2017; Shi et al, 2015). It has been demonstrated in some studies that lncRNA UCA1 can regulate the proliferation of bladder cancer cells by acting on the PI3K‐AKT‐mTOR signaling pathway. It was found that lncRNA NORAD exhibits an obvious high expression in NSCLC, so it was expected to further explore the role of NORAD in NSCLC and its potential mechanism
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