Evidence map›Paper›PMID 26991540›Full record

ArticleJournal of cellular and molecular medicine2016

Suppressive action of miRNAs to ARP2/3 complex reduces cell migration and proliferation via RAC isoforms in Hirschsprung disease.

Weibing Tang, Peng Cai, Weiwei Huo, Hongxing Li, Junwei Tang, Dongmei Zhu, Hua Xie, Pingfa Chen, Bo Hang, Shouyu Wang and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2016. 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 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 12% 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, 29 citations in OpenAlex.

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  12. MicroRNA-4516-mediated regulation ofJournal of medical genetics · 2020
    Article
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  15. Pharmacogenomics and personalized medicine · 2020
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  17. Corrigendum.Journal of cellular and molecular medicine · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Weibing TangDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated Nanjing Medical University, Nanjing, China.
Peng CaiChildren's Hospital of Soochow University, Soochow, China.
Weiwei HuoState Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing, China.
Hongxing LiDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated Nanjing Medical University, Nanjing, China.
Junwei TangDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated Nanjing Medical University, Nanjing, China.
Dongmei ZhuDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated Nanjing Medical University, Nanjing, China.
Hua XieDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated Nanjing Medical University, Nanjing, China.
Pingfa ChenDepartment of Pediatric Surgery, Nanjing Children's Hospital Affiliated Nanjing Medical University, Nanjing, China.
Bo HangDepartment of Cell and Molecular Biology, Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.
Shouyu WangState Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing, China.
Yankai XiaChildren's Hospital of Soochow University, Soochow, China.
Nanjing Medical University · CNNanjing Children's Hospital · CNLawrence Berkeley National Laboratory · USSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hirschsprung disease (HSCR) is a congenital disorder caused by the defective function of the embryonic enteric neural crest. The impaired migration of embryonic enteric neural crest plays an important role in the pathogenesis of this disease. Recent studies showed that the ARP2/3 complex and RAC isoforms had effects on actin cytoskeleton remodelling, which contributes to migration. Moreover, some regulatory relationships were identified between ARP2/3 complex and RAC isoforms. Although microRNAs (miRNAs) have been known to modulate target gene expression on the post-transcriptional level, little is known about the regulation among miRNAs, ARP2/3 complex and RAC isoforms. Here, we report that down-regulation of ARP2 and ARP3, two main subunits of ARP2/3 complex, suppressed migration and proliferation in 293T and SH-SY5Y cell lines via the inhibition of RAC1 and RAC2. Meanwhile, as the target genes, ARP2 and ARP3 are reduced by increased miR-24-1* and let-7a*, respectively, in 70 HSCR samples as compared with 74 normal controls. Co-immunoprecipitation showed that aberrant reduction in ARP2 and ARP3 could weaken the function of ARP2/3 complex. Our study demonstrates that the miR-24-1*/let-7a*-ARP2/3 complex-RAC isoforms pathway may represent a novel pathogenic mechanism for HSCR.

Indexed as

Cell MovementActin-Related Protein 2-3 ComplexBase SequenceCell Line, TumorCell ProliferationDemographyDown-RegulationFemaleHirschsprung DiseaseHumansImmunoprecipitationInfantMaleMicroRNAsModels, BiologicalProtein IsoformsActin-Related Protein 2-3 ComplexMicroRNAsMIRN24 microRNA, humanmirnlet7 microRNA, humanProtein Isoformsrac1 GTP-Binding ProteinRAC1 protein, humanRAC2 GTP-Binding Proteinrac GTP-Binding ProteinsRNA, MessengerARP2/3 complexgene regulationHirschsprung diseasemicroRNARAC isoforms

Identifiers

PMID26991540
PMCPMC4929290
OpenAlexW2299313456

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.