ArticleMolecular medicine reports2021
NORAD regulates epithelial‑mesenchymal transition of non‑small cell lung cancer cells via miR‑422a.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Article
- NORAD modulates miR-30c-5p-LDHA to protect lung endothelial cells damage.Open medicine (Warsaw, Poland) · 2022Article
- Non-coding RNA Activated by DNA Damage: Review of Its Roles in the Carcinogenesis.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
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