Evidence map›Paper›PMID 25481483›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2014

MiR-210 up-regulation inhibits proliferation and induces apoptosis in glioma cells by targeting SIN3A.

Chao Shang, Yang Hong, Yan Guo, Yun-hui Liu, Yi-xue Xue

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  12. Hypoxia-Induced Non-Coding RNAs Controlling Cell Viability in Cancer.International journal of molecular sciences · 2021
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  18. MiR-210 inhibits hypoxia-induced apoptosis of smooth muscle cells via targeting MEF2C.International journal of clinical and experimental pathology · 2019
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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

5 authors at 1 institution in 1 country.

Chao ShangDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning, China (mainland).
Yang HongDepartment of Neurosurgery, Shengjing Hospital, China Medical University, Shenyang, Liaoning, China (mainland).
Yan GuoDepartment of Central Laboratory, School of Stomatology, China Medical University, Shenyang, Liaoning, China (mainland).
Yun-hui LiuDepartment of Neurosurgery, Shengjing Hospital, China Medical University, Shenyang, Liaoning, China (mainland).
Yi-xue XueDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning, China (mainland).
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aim of this study was to determine whether miR-210 can affect the apoptosis and proliferation of human U251 glioma cells from down-regulating SIN3A. MATERIAL AND

methodsThe expression of miRNA-210 was detected by quantitative real-time PCR in normal brain tissue and glioma samples. The apoptosis and proliferation ability of U251 cells were analyzed by MTT and flow cytometry assay after anti-miR-210 transfection. For the regulation mechanism analysis of miR-210, TargetScan, PicTar, and microRNA were selected to predict some potential target genes of miR-210. The predicted gene was identified to be the direct and specific target gene of miR-210 by luciferase activities assay and Western blot. RNA interference technology was used to confirm that the apoptosis and proliferation effects of miR-210 were directly induced by SIN3A.

resultsThe expression of miR-210 increased significantly in glioma in comparison with normal brain tissue. The silence of miR-210 expression could inhibit the proliferation of U251 cells and induce the apoptosis. Mechanism analysis revealed that SIN3A was a specific and direct target gene of miR-210. The siRNA-SIN3A could down-regulate the expression of SIN3A protein, which was up-regulated in U251 cells by anti-miR-210 transfection, and our experiments found that silence of SIN3A could inhibit the apoptosis and sharply increase the proliferation of U251 cells. The regulation effects of anti-miR-210 on apoptosis and proliferation can be reversed respectively by the expression silence of SIN3A.

conclusionsAberrantly expressed miR-210 regulates human U251 glioma cells apoptosis and proliferation partly through directly down-regulating SIN3A protein expression. This might offer a new potential therapeutic stratagem for glioma.

Indexed as

3' Untranslated RegionsAgedApoptosisBase SequenceBrain NeoplasmsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticGliomaHumansMaleMicroRNAsMiddle AgedMolecular Sequence DataReal-Time Polymerase Chain Reaction3' Untranslated RegionsMicroRNAsMIRN210 microRNA, humanRepressor ProteinsSIN3A transcription factorSin3 Histone Deacetylase and Corepressor Complex

Identifiers

PMID25481483
PMCPMC4266365
OpenAlexW2110402883

What OpenQuestion holds

Textmetadata
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.