Open Access

NORAD regulates epithelial‑mesenchymal transition of non‑small cell lung cancer cells via miR‑422a

Corrigendum in: /10.3892/mmr.2021.12178

  • Authors:
    • Zhikun Chen
    • Qin Che
    • Chunxue Xie
  • View Affiliations

  • Published online on: December 3, 2020     https://doi.org/10.3892/mmr.2020.11750
  • Article Number: 111
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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.
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February-2021
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Spandidos Publications style
Chen Z, Che Q and Xie C: NORAD regulates epithelial‑mesenchymal transition of non‑small cell lung cancer cells via miR‑422a Corrigendum in /10.3892/mmr.2021.12178. Mol Med Rep 23: 111, 2021
APA
Chen, Z., Che, Q., & Xie, C. (2021). NORAD regulates epithelial‑mesenchymal transition of non‑small cell lung cancer cells via miR‑422a Corrigendum in /10.3892/mmr.2021.12178. Molecular Medicine Reports, 23, 111. https://doi.org/10.3892/mmr.2020.11750
MLA
Chen, Z., Che, Q., Xie, C."NORAD regulates epithelial‑mesenchymal transition of non‑small cell lung cancer cells via miR‑422a Corrigendum in /10.3892/mmr.2021.12178". Molecular Medicine Reports 23.2 (2021): 111.
Chicago
Chen, Z., Che, Q., Xie, C."NORAD regulates epithelial‑mesenchymal transition of non‑small cell lung cancer cells via miR‑422a Corrigendum in /10.3892/mmr.2021.12178". Molecular Medicine Reports 23, no. 2 (2021): 111. https://doi.org/10.3892/mmr.2020.11750