NORAD regulates epithelial‑mesenchymal transition of non‑small cell lung cancer cells via miR‑422a
- Zhikun Chen
- Qin Che
- Chunxue Xie
Affiliations: Department of Emergency, Jingmen No. 1 People's Hospital, Jingmen, Hubei 448000, P.R. China, Department of Infectious Diseases, Jingmen No. 1 People's Hospital, Jingmen, Hubei 448000, P.R. China, Department of General Practice, Jingmen No. 1 People's Hospital, Jingmen, Hubei 448000, P.R. China
- Published online on: December 3, 2020 https://doi.org/10.3892/mmr.2020.11750
Copyright: © Chen
et al. This is an open access article distributed under the
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The poor prognosis of non‑small cell lung cancer (NSCLC) is related to epithelial‑mesenchymal transition (EMT). Recent studies demonstrated that non‑coding RNA activated by DNA damage (NORAD) displays a carcinogenic effect and targets microRNA (miR)‑422a, which may be involved in tumor cell migration and invasion. The aim of the present study was to investigate the effect of NORAD on NSCLC cell EMT and the underlying mechanism. Reverse transcription‑quantitative PCR and western blotting were performed to detect the expression levels of long non‑coding RNAs, miRNAs and mRNAs. Cell viability, migration and invasion were detected by conducting Cell Counting Kit‑8, wound healing and Transwell assays, respectively. The target of NORAD was predicted using starBase and further confirmed by conducting a dual‑luciferase reporter assay. The results indicated that NORAD expression was significantly increased in lung cancer tissues and cells compared with adjacent healthy tissues and cells. Compared with the control groups, NORAD overexpression promoted SK‑MES‑1 cell viability, migration and invasion, whereas NORAD knockdown resulted in the opposite effects in A549 cells. Moreover, miR‑422a, which was predicted to be a target of NORAD, displayed lower expression levels in lung cancer tissues compared with adjacent healthy tissues. In addition, miR‑422a overexpression partially reversed NORAD overexpression‑induced increases in SK‑MES‑1 cell viability, migration, invasion and EMT. In addition, miR‑422a knockdown partially reversed the effects of NORAD knockdown. The present study suggested that NORAD regulated lung cancer cell EMT by regulating the expression of miR‑422a, providing a potential therapeutic target for the intervention of the development of NSCLC.