Evidence map›Paper›PMID 26274316›Full record

ArticlePloS one2015

VEGFA Expression Is Inhibited by Arsenic Trioxide in HUVECs through the Upregulation of Ets-2 and miRNA-126.

Hong-Yan Ge, Zhong-Jing Han, Pei Tian, Wen-Jie Sun, Da-Xi Xue, Yu Bi, Zhang-Hui Yang, Ping Liu

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
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  10. Drug repurposing in malignant pleural mesothelioma: a breath of fresh air?European respiratory review : an official journal of the European Respiratory Society · 2018
    Review
  11. Article
  12. Article
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

8 authors.

Hong-Yan GeKey Laboratory of Harbin Medical University Eye Center, Eye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Harbin, China.
Zhong-Jing HanDaqing Oilfield General Hospital,9 ZhongKang street, Saertu District of Daqing, China; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Pei TianKey Laboratory of Harbin Medical University Eye Center, Eye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Harbin, China.
Wen-Jie SunKey Laboratory of Harbin Medical University Eye Center, Eye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Harbin, China; Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Key Laboratory of Myocardial Ischemia Mechanism and Treatment (Harbin Medical University), Ministry of Education, Baojian Road, Harbin, Heilongjiang Province, PR China.
Da-Xi XueKey Laboratory of Harbin Medical University Eye Center, Eye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Harbin, China.
Yu BiKey Laboratory of Harbin Medical University Eye Center, Eye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Harbin, China.
Zhang-Hui YangKey Laboratory of Harbin Medical University Eye Center, Eye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Harbin, China.
Ping LiuKey Laboratory of Harbin Medical University Eye Center, Eye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Harbin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arsenic trioxide (ATO) has been used to treat patients with acute promyelocytic leukemia. Recently, studies have shown that ATO can induce apoptosis in leukemic cells and blood vessel endothelial cells in a time- and dose-dependent manner through the inhibition of vascular endothelial growth factor A (VEGFA) production. VEGFA is a key factor in angiogenesis initiation. Targeted inhibition of VEGF or VEGFA expression can suppress angiogenesis; however, little is known about the mechanism by which ATO inhibits VEGFA expression. In this study, we investigated the role of miRNA-126 in the mechanism of action of ATO in human umbilical vein endothelial cells (HUVECs). ATO significantly decreased the viability and proliferation of HUVECs and decreased their migration at 48 h. Cell proliferation was inhibited by 50% (IC50) when 5.0 μmol/L ATO was used. ATO treatment induced miR-126 upregulation and HUVEC apoptosis. Transfection with a miR-126 mimic significantly downregulated VEGFA mRNA levels, and transfection with a miR-126 inhibitor significantly upregulated VEGFA mRNA levels. Finally, we showed that ATO treatment upregulated Ets-2 and miR-126 expression in HUVECs. These results demonstrate that ATO inhibits the growth of HUVECs and induces apoptosis by downregulating VEGFA. One mechanism by which this occurs is Ets-2 upregulation, which results in an increase in miR-126 levels and downregulation of VEGFA expression.

Indexed as

ApoptosisArsenicalsArsenic TrioxideCell MovementCell ProliferationCell SurvivalDown-RegulationHumansHuman Umbilical Vein Endothelial CellsMicroRNAsOxidesProto-Oncogene Protein c-ets-2Up-RegulationVascular Endothelial Growth Factor AArsenicalsArsenic TrioxideETS2 protein, humanMicroRNAsMIRN126 microRNA, humanOxidesProto-Oncogene Protein c-ets-2Vascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID26274316
PMCPMC4537190

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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.