Evidence map›Paper›PMID 24376632›Full record

ArticlePloS one2013

MicroRNA-155 promotes glioma cell proliferation via the regulation of MXI1.

Jianwen Zhou, Wei Wang, Zhenhua Gao, Xueling Peng, Xulin Chen, Wei Chen, Weiyi Xu, Haixiong Xu, Marie C Lin, Songshan Jiang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 61 citations in OpenAlex.

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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 5 institutions in 1 country.

Jianwen ZhouState Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China ; Key Laboratory of Gene Engineering of the Ministry of Education, School of Life Sciences, Sun Yat-sen University, Guangzhou, China ; Department of Pathology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Wei WangNeurosurgery Department, Epilepsy Centre, Guangzhou General Hospital, Guangzhou Command, PLA, Guangzhou, China ; HuaBo Bio-Pharmaceutic Institute of Guangzhou, Guangzhou, China.
Zhenhua GaoDepartment of Radiology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Xueling PengState Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China ; Shenzhen State High-Tech Industrial Innovation Centre, Shenzhen, China.
Xulin ChenKey Laboratory of Gene Engineering of the Ministry of Education, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Wei ChenDepartment of Gynecology, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Weiyi XuState Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Haixiong XuDepartment of Neurosurgery, Affiliated Shantou Hospital of Sun Yat-sen University, Shantou, China.
Marie C LinBiomedical Eng. Res. Center, Kunming Medical University, Kunming, China.
Songshan JiangState Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China ; Key Laboratory of Gene Engineering of the Ministry of Education, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNGeneral Hospital of Guangzhou Military Command · CNGuangzhou Medical University · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliomas are the most common and aggressive primary tumors in the central nervous system. Recently, Max interactor-1 (MXI1), an antagonist of c-Myc that is involved in brain tumor progression, has been reported to be deregulated in a variety of tumors including glioma. However, the mechanism of MXI1 deregulation in gliomas remains unclear. In this study, we show that the relative expression level of MXI1 is markedly down-regulated in glioma cell lines. Using integrated bioinformatic analysis and experimental confirmation, we identified several miRNAs by screening a panel of predicted miRNAs that may regulate the MXI1 3'UTR. The strongest inhibitory miRNA, miR-155, can attenuate the activity of a luciferase reporter gene that is fused with the MXI1 3'UTR and decrease the expression levels of MXI1 mRNA and protein in U87 glioma cells. The potential role of miR-155 in promoting glioma cell proliferation by targeting MXI1 was confirmed in various glioma cell lines by rescue experiments using MTT assays, EdU incorporation assay, and cell counting experiments. In addition, we determined that the level of MXI1 mRNA was inversely correlated with the expression of miR-155 in 18 sets of glioblastoma multiforme specimens. These findings reveal for the first time that the targeting of MXI1 by miR-155 may result in a reduction in MXI1 expression and promote glioma cell proliferation; this result suggests a novel function of miR-155 in targeting MXI1 in glioma-genesis.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsBase SequenceBasic Helix-Loop-Helix ProteinsBrain NeoplasmsCell Line, TumorCell ProliferationEpigenesis, GeneticGenes, ReporterGlioblastomaHumansLuciferasesMicroRNAsMolecular Sequence DataTumor Suppressor Proteins3' Untranslated RegionsBasic Helix-Loop-Helix ProteinsLuciferasesMicroRNAsMIRN155 microRNA, humanMXI1 protein, humanTumor Suppressor Proteins

Identifiers

PMID24376632
PMCPMC3871643
OpenAlexW2063568763

What OpenQuestion holds

Textmetadata
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.