Evidence map›Paper›PMID 31819489›Full record

ArticleOncoTargets and therapy2019

RRM2 Regulated By LINC00667/miR-143-3p Signal Is Responsible For Non-Small Cell Lung Cancer Cell Progression.

Yanbing Yang, Sensen Li, Juan Cao, Yaojun Li, Haiying Hu, Zhuyu Wu

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. LINC00667: A Novel Vital Oncogenic LincRNA.Current medicinal chemistry · 2025
    Review
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  5. Review
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  9. GINS2 promotes the progression of human HNSCC by altering RRM2 expression.Cancer biomarkers : section A of Disease markers · 2024
    Article
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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

6 authors at 1 institution in 1 country.

Yanbing Yang *Department of Respiratory Medicine, Luohe Central Hospital, The First Affiliated Hospital of Luohe Medical College, Luohe, Henan 462000, People's Republic of China.
Sensen Li *Department of Pharmacy, Luohe Central Hospital, The First Affiliated Hospital of Luohe Medical College, Luohe, Henan 462000, People's Republic of China.
Juan CaoDepartment of Respiratory Medicine, Luohe Central Hospital, The First Affiliated Hospital of Luohe Medical College, Luohe, Henan 462000, People's Republic of China.
Yaojun LiDepartment of Respiratory Medicine, Luohe Central Hospital, The First Affiliated Hospital of Luohe Medical College, Luohe, Henan 462000, People's Republic of China.
Haiying HuDepartment of Respiratory Medicine, Luohe Central Hospital, The First Affiliated Hospital of Luohe Medical College, Luohe, Henan 462000, People's Republic of China.
Zhuyu WuDepartment of Respiratory Medicine, Luohe Central Hospital, The First Affiliated Hospital of Luohe Medical College, Luohe, Henan 462000, People's Republic of China.
Luohe Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is a common and fatal cancer worldwide with a very low 5-year overall survival rate. Ribonucleotide reductase M2 subunit (RRM2), a small subunit of the ribonucleotide reductase complex, has been found to be an oncogenic role in a variety of tumors including NSCLC. However, the regulatory mechanism of RRM2 in NSCLC is not clear. Increasing evidence suggests that non-coding RNAs (ncRNAs) including miRNAs and lincRNAs may promote or inhibit tumor initiation and development through regulating the expression of oncogenic genes. It is interesting to find ncRNAs which play important role in regulating RRM2 expression. MATERIALS AND

methodsThe expression levels of RRM2, LINC0066 and miR-143-3p in NSCLC tumor tissues and cell lines were detected using qRT-PCR. The regulatory relationships among RRM2, LINC0066 and miR-143-3p were predicted using database analysis and verified by luciferase reporter assay and RIP analysis. The proliferation ability of NSCLC cells was assessed using CCK8 and colony formation assays. The expression of related proteins was determined by Western blot. In vivo effect of RRM2, LINC0066 and miR-143-3p to NSCLC were detected through xenograft experiments.

resultsIn this study, we found RRM2 was upregulated in NSCLC tumor and cell lines, and the aberrant upregulation predicted a poor prognosis. Then, we predicted and confirmed that RRM2 was negatively regulated by miR-143-3p. Further study implied that LINC00667 acted as a ceRNA by sponging miR-143-3p and regulated RRM2 expression indirectly. Moreover, we found that the growth of NSCLC was regulated by LINC00667/miR-143-3p/RRM2 signal pathway both in vitro and in vivo. LINC00667 and RRM2 promoted the tumor growth while miR-143-3p inhibited it.

conclusionOur study revealed a LINC00667/miR-143-3p/RRM2 signal pathway that played an important role in the progress of NSCLC, which might be potential therapeutic targets for NSCLC.

Indexed as

LINC00667miR-143-3pNSCLCRRM2

Identifiers

PMID31819489
PMCPMC6876211
OpenAlexW2989970146

What OpenQuestion holds

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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.