Evidence map›Paper›PMID 33311443›Full record

ArticleCell death & disease2020

Linc00426 accelerates lung adenocarcinoma progression by regulating miR-455-5p as a molecular sponge.

Hongli Li, Qingjie Mu, Guoxin Zhang, Zhixin Shen, Yuanyuan Zhang, Jun Bai, Liping Zhang, Dandan Zhou, Quan Zheng, Lihong Shi and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

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  14. NF-Journal of oncology · 2022
    Article
  15. Article
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  17. [MiR-671-5p negatively regulates SMAD3 to inhibit migration and invasion of osteosarcoma cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Hongli LiExperimental Center for Medicine Research, Weifang Medical University, 261053, Weifang, China.
Qingjie MuSchool of Clinical Medicine, Weifang Medical University, 261053, Weifang, China.
Guoxin ZhangCollege of Biological Science and Technology, Weifang Medical University, 261053, Weifang, China.
Zhixin ShenDepartment of Clinical Surgery, Affiliated Hospital of Weifang Medical University, 261053, Weifang, China.
Yuanyuan ZhangCollege of Nursing, Weifang Medical University, 261053, Weifang, China.
Jun BaiDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, 261053, Weifang, China.
Liping ZhangDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, 261053, Weifang, China.
Dandan ZhouDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, 261053, Weifang, China.
Quan ZhengDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, 261053, Weifang, China.
Lihong ShiSchool of Clinical Medicine, Weifang Medical University, 261053, Weifang, China.
Wenxia SuSchool of Clinical Medicine, Weifang Medical University, 261053, Weifang, China.
Chonggao YinCollege of Nursing, Weifang Medical University, 261053, Weifang, China. yinchg@wfmc.edu.cn.
Baogang ZhangDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, 261053, Weifang, China. zhangbg@wfmc.edu.cn.
Weifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing lines of evidence indicate the role of long non-coding RNAs (LncRNAs) in gene regulation and tumor development. Hence, it is important to elucidate the mechanisms of LncRNAs underlying the proliferation, metastasis, and invasion of lung adenocarcinoma (LUAD). We employed microarrays to screen LncRNAs in LUAD tissues with and without lymph node metastasis and revealed their effects on LUAD. Among them, Linc00426 was selected for further exploration in its expression, the biological significance, and the underlying molecular mechanisms. Linc00426 exhibits ectopic expression in LUAD tissues and cells. The ectopic expression has been clinically linked to tumor size, lymphatic metastasis, and tumor differentiation of patients with LUAD. The deregulation of Linc00426 contributes to a notable impairment in proliferation, invasion, metastasis, and epithelial-mesenchymal transition (EMT) in vitro and in vivo. Mechanistically, the deregulation of Linc00426 could reduce cytoskeleton rearrangement and matrix metalloproteinase expression. Meanwhile, decreasing the level of Linc00426 or increasing miR-455-5p could down-regulate the level of UBE2V1. Thus, Linc00426 may act as a competing endogenous RNA (ceRNA) to abate miR-455-5p-dependent UBE2V1 reduction. We conclude that Linc00426 accelerates LUAD progression by acting as a molecular sponge to regulate miR-455-5p, and may be a potential novel tumor marker for LUAD.

Indexed as

Disease ProgressionGene Expression Regulation, NeoplasticAdenocarcinoma of LungAnimalsBase SequenceBinding, CompetitiveCell Line, TumorCell ProliferationCytoskeletonDown-RegulationEpithelial-Mesenchymal TransitionFemaleHumansLung NeoplasmsLymphatic MetastasisMaleMatrix MetalloproteinasesMicroRNAsMIRN455 microRNA, humanRNA, Long NoncodingTranscription FactorsUBE2V1 protein, humanUbiquitin-Conjugating Enzymes

Identifiers

PMID33311443
PMCPMC7732829
OpenAlexW3111109452

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.