Evidence map›Paper›PMID 26956882›Full record

ArticleLipids in health and disease2016

MiR-106b exhibits an anti-angiogenic function by inhibiting STAT3 expression in endothelial cells.

Ailifeire Maimaiti, Aikebaier Maimaiti, Yining Yang, Yitong Ma

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  6. MicroRNAs and Heat Shock Proteins in Breast Cancer Biology.Methods in molecular biology (Clifton, N.J.) · 2022
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  10. Frontiers in genetics · 2021
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  13. Review
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  15. Article
  16. MicroRNA profiling of diabetic atherosclerosis in a rat model.European journal of medical research · 2018
    Article
  17. Article
  18. Effect of miR-106b on Invasiveness of Pituitary Adenoma via PTEN-PI3K/AKT.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Ailifeire MaimaitiThe Heart Center, the First Affiliated Hospital of Xinjiang Medical University, No.137 Liyushan South Road, Urumqi, Xinjiang, China. alfira.md@foxmail.com.
Aikebaier MaimaitiThe Heart Center, the First Affiliated Hospital of Xinjiang Medical University, No.137 Liyushan South Road, Urumqi, Xinjiang, China. 39404459@qq.com.
Yining YangThe Heart Center, the First Affiliated Hospital of Xinjiang Medical University, No.137 Liyushan South Road, Urumqi, Xinjiang, China. yangyn5126@163.com.
Yitong MaThe Heart Center, the First Affiliated Hospital of Xinjiang Medical University, No.137 Liyushan South Road, Urumqi, Xinjiang, China. myt-xj@163.com.
Xinjiang Medical University · CNFirst Affiliated Hospital of Xinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent discoveries of the atherosclerosis-related miRNAs shed new light on the treatment of cardiovascular diseases. Of note, miR-106b ~ 25 cluster and miR-17 ~ 92 cluster are paralogs. Up till now, plenty of researches have shown the role of miR-17 ~ 92 cluster in tumor and atherosclerosis, but miR-106b ~ 25 cluster has stayed mysterious in atherosclerosis field. This study was designed to investigate how miR-106b functions in the atherosclerosis-related angiogenesis and to explore the functioning processes of miR-106b, so as to seek out a new target for the treatment of atherosclerosis.

methodsUp and down regulation of miR-106b expression was achieved through transfection in HUVECs so as to investigate the function of miR-106b. Next we predicted the target genes of miR-106b and detected them using qRT-PCR and Western blot technique. At last, luciferase assay was conducted to verify the direct target gene of miR-106b. Data are expressed as mean ± SEM. Two treatment groups were compared by Mann-Whitney U test or student's t-test. Results were considered statistically significant when P < 0.05.

resultsThe results showed miR-106b up-regulation groups formed less tubes than control groups while the down-regulation groups showed the opposite. Meanwhile, no obvious effect on apoptosis was observed in endothelial cells. Next we predicted the target genes of miR-106b and finally settled down to MAPK14 (Mitogen-Activated Protein Kinase), STAT3 (Signal Transducers and Activators of Transcription 3), JAK1(Janus Kinase 1) and VEGFA(Vascular Endothelial Growth Factor A) as candidate target genes. Our results revealed over-expressed miR-106b represses STAT3 expression, while miR-106b inhibition resulted in STAT3 up-regulation. Ultimately, luciferase assay confirmed STAT3 mRNA is the direct target of miR-106b.

conclusionsOur research demonstrated that miR-106b modulate angiogenesis in endothelial cells through affecting expression of STAT3, which occurs by direct target action. Therefore, we affirmed that miR-106b exerts an anti-angiogenic effect in endothelial cells via STAT3-involved signaling pathway, via directly targeting STAT3.

Indexed as

Flow CytometryHumansHuman Umbilical Vein Endothelial CellsMicroRNAsSTAT3 Transcription FactorMicroRNAsMIRN106 microRNA, humanSTAT3 Transcription Factor

Identifiers

PMID26956882
PMCPMC4784424
OpenAlexW2294901556

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.