Evidence map›Paper›PMID 31207175›Full record

ArticleMolecular genetics & genomic medicine2019

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

Tianyu Chen, Shaoyun Qin, Yinan Gu, Huaqin Pan, Dachen Bian

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 40 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Tianyu ChenDepartment of Respiratory Medicine, Jiangsu Taizhou People's Hospital, Taizhou, China.ORCID 0000-0003-3314-365X
Shaoyun QinDepartment of Respiratory Medicine, Jiangsu Taizhou People's Hospital, Taizhou, China.
Yinan GuDepartment of Respiratory Medicine, Jiangsu Taizhou People's Hospital, Taizhou, China.
Huaqin PanDepartment of Respiratory Medicine, Jiangsu Taizhou People's Hospital, Taizhou, China.
Dachen BianDepartment of Respiratory Medicine, Jiangsu Taizhou People's Hospital, Taizhou, China.
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

A549 CellsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansLung NeoplasmsMicroRNAsProto-Oncogene Proteins c-aktRNA, Long NoncodingAKT1 protein, humanMicroRNAsMIRN656 microRNA, humanNORAD long non-coding RNA, humanProto-Oncogene Proteins c-aktRNA, Long NoncodingAKT1long non-coding RNAmiR-656-3pnon-small cell lung cancerNORAD

Identifiers

PMID31207175
PMCPMC6712722
OpenAlexW2949944784

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.