Evidence map›Paper›PMID 33628829›Full record

ArticleBioMed research international2021

miR-193a-3p Promotes the Invasion, Migration, and Mesenchymal Transition in Glioma through Regulating BTRC.

Dan-Dan Zhou, Hong-Li Li, Wei Liu, Li-Ping Zhang, Quan Zheng, Jun Bai, Ya-Qiong Hu, Chong-Gao Yin, Shi-Jun Lv, Bao-Gang Zhang

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

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  9. [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
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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

10 authors at 1 institution in 1 country.

Dan-Dan ZhouDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261053, China.
Hong-Li LiDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261053, China.
Wei LiuSchool of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261053, China.
Li-Ping ZhangDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261053, China.
Quan ZhengDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261053, China.
Jun BaiDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261053, China.
Ya-Qiong HuDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261053, China.
Chong-Gao YinCollege of Nursing, Weifang Medical University, Weifang, Shandong 261053, China.
Shi-Jun LvDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261053, China.ORCID https://orcid.org/0000-0002-0945-2340
Bao-Gang ZhangDepartment of Pathology, School of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261053, China.ORCID https://orcid.org/0000-0002-2355-6461
Weifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe present study is aimed at exploring the specific expression of miR-193a-3p and the mechanism underlying miR-193a-3p-mediated mesenchymal transition (MT), invasion, and migration in glioma.

methodsThe gene expression profile datasets of GSE39486 and GSE25676 were downloaded from the National Center for Biotechnology (NCBI). Data regarding the expression of miR-193a-3p and survival curves were derived from Chinese Glioma Genome Atlas (CGGA). Online websites including miRWalk, DIANA, and starbase were employed to predict the target genes for miR-193a-3p. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed by the Omicsbean online software. Module analysis of the protein-protein interaction (PPI) networks was performed by the plug-in Molecular Complex Detection (MCODE), and the degrees of genes were calculated by CytoHubba plug-in of Cytoscape. Survival curves were based on the Gene Expression Profile Interaction Analysis (GEPIA). Transwell, wound healing, and Western blot experiments were performed to investigate the effects of miR-193a-3p and beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC) on the invasion, migration, and MT of glioma.

resultsmiR-193a-3p was highly expressed in glioma tissues and significantly correlated with poor survival in patients with glioma. The target genes for miR-193a-3p were involved in many cancer-related signaling pathways. The PPI showed 11 genes with both high degrees and MCODE scores in the network. Survival analysis demonstrated that the expression of BTRC was significantly correlated with the prognosis of patients with glioma. The results from the transwell, wound healing, and Western blot analyses suggested that miR-193a-3p promoted the invasion, migration, and MT of glioma cells, which could be reversed by BTRC.

conclusionsmiR-193a-3p was upregulated in patients with glioma and could affect the invasion, migration, and MT of glioma by regulating BTRC.

Indexed as

beta-Transducin Repeat-Containing ProteinsBrain NeoplasmsGliomaMicroRNAsBrainCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHumansNeoplasm InvasivenessPrognosisProtein Interaction MapsTranscriptomebeta-Transducin Repeat-Containing ProteinsBTRC protein, humanMicroRNAsMIRN193 microRNA, human

Identifiers

PMID33628829
PMCPMC7886567
OpenAlexW3128293704

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.