Retracted: Long non‐coding RNA NORAD promotes the occurrence and development of non‐small cell lung cancer by adsorbing MiR‐656‐3p

Abstract

Background To 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. Methods Quantitative 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. Results The 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. Conclusion LncRNA 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.

Long noncoding RNA VPS9D1-AS1 augments the malignant phenotype of non-small cell lung cancer by sponging microRNA-532-3p and thereby enhancing HMGA2 expression

“…LncRNAs function as guides, scaffolds, and molecular sponges in their interactions with proteins, microRNAs (miRNAs), and mRNAs, thereby creating complex networks that regulate various physiological and pathological processes, including cancer initiation and progression [8]. Recently, several studies revealed the contribution of lncRNAs to the formation and progression of multiple types of cancers, including NSCLC [9][10][11]. A large number of lncRNAs are expressed abnormally in NSCLC, e.g., HOXA-AS2 [12], LEF1-AS1 [13], and BLACAT1 [14].…”

LncRNA SNHG14 contributes to the progression of NSCLC through miR‐206/G6PD pathway

“…The role of lncRNA NORAD in NSCLC was discovered by Chen et al . in promoting the development of lung cancer . However, the role of lncRNA SNHG14 in lung cancer remains unclear.…”

Retracted Article: Long noncoding RNA ANRIL knockdown increases sensitivity of non-small cell lung cancer to cisplatin by regulating the miR-656-3p/SOX4 axis

“…15 A novel miRNA miR-656-3p has been regarded as a tumor suppressor in glioma and NSCLC. 16,17 However, little is known about the role of this miRNA in CDDP resistance in NSCLC. Sex-determining region Y-related highmobility group box (SOX) family has key roles in tumorigenesis and metastasis of human cancers.…”