Evidence map›Paper›PMID 32055266›Full record

ArticleInternational journal of clinical and experimental pathology2020

Long noncoding RNA NORAD regulates lung cancer cell proliferation, apoptosis, migration, and invasion by the miR-30a-5p/ADAM19 axis.

Jun Li, Xia Xu, Cungang Wei, Lei Liu, Tengqi Wang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. ADAM19: biological characteristics and implications in disease pathology and clinical applications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Jun LiDepartment of Thoracic Surgery, Bayannaoer City Hospital Inner Mongolia, China.
Xia XuDepartment of Gynaecology and Obstetrics, Dengkou County People Hospital Inner Mongolia, China.
Cungang WeiDepartment of Thoracic Surgery, Bayannaoer City Hospital Inner Mongolia, China.
Lei LiuDepartment of Thoracic Surgery, Bayannaoer City Hospital Inner Mongolia, China.
Tengqi WangDepartment of Oncology, Bayannaoer City Hospital Inner Mongolia, China.
Inner Mongolia People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer is one of the most common human cancers. Long noncoding RNA-activated by DNA damage (NORAD) is often upregulated and promotes cell progression in various human cancers; however, its function and possible mechanism in lung cancer remain largely unknown.

methodsThe expression levels of NORAD, miR-30a-5p and a disintegrin and metalloproteinase 19 (ADAM19) were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4, 5)-dimethylthiazole-2-y1)-2, 5-biphenyl tetrazolium bromide (MTT) assay, flow cytometry, and transwell assay were employed to detect cell proliferation, apoptosis, migration, and invasion abilities, respectively. Western blot was used to detect the protein expression of ADAM19. The interaction between miR-30a-5p and NORAD or ADAM19 was predicted by online software and confirmed by the dual-luciferase reporter assay.

resultsThe expression levels of NORAD and ADAM19 were increased and the expression level of miR-30a-5p was decreased in lung cancer tissues and cells. Knockdown of NORAD could inhibit cell proliferation, migration and invasion but promote apoptosis in lung cancer cells. In addition, NORAD directly interacted with miR-30a-5p and its overexpression reversed the anti-cancer role of miR-30a-5p in lung cancer. Moreover, miR-30a-5p directly targeted ADAM19 and its inhibition attenuated the inhibitory effect of ADAM19 knockdown on progression of lung cancer cells. Furthermore, NORAD functioned as a competing endogenous RNA (ceRNA) through sponging miR-30a-5p to regulate ADAM19 expression.

conclusionNORAD knockdown suppressed cell proliferation, migration and invasion but promoted cell apoptosis in lung cancer cells by regulating miR-30a-5p/ADAM19, providing a possible therapeutic strategy for lung cancer patients.

Indexed as

ADAM19cell progressionLung cancermiR-30a-5pNORAD

Identifiers

PMID32055266
PMCPMC7013373
OpenAlexW3009961267

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.