Evidence map›Paper›PMID 26046465›Full record

ArticleOncotarget2015

Analysis of the transcriptional regulation of cancer-related genes by aberrant DNA methylation of the cis-regulation sites in the promoter region during hepatocyte carcinogenesis caused by arsenic.

Zhuang Miao, Lin Wu, Ming Lu, Xianzhi Meng, Bo Gao, Xin Qiao, Weihui Zhang, Dongbo Xue

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  6. Review
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  8. Review
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  10. Paradoxical effects of arsenic in the lungs.Environmental health and preventive medicine · 2021
    Review
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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

8 authors at 3 institutions in 2 countries.

Zhuang MiaoDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, PR China.
Lin WuDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, PR China.
Ming LuDepartment of Surgery, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA, USA.
Xianzhi MengDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, PR China.
Bo GaoDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, PR China.
Xin QiaoDepartment of Surgery, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA, USA.
Weihui ZhangDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, PR China.
Dongbo XueDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, PR China.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CNUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver is the major organ for arsenic methylation metabolism and may be the potential target of arsenic-induced cancer. In this study, normal human liver cell was treated with arsenic trioxide, and detected using DNA methylation microarray. Some oncogenes, tumor suppressor genes, transcription factors (TF), and tumor-associated genes (TAG) that have aberrant DNA methylation have been identified. However, simple functional studies of genes adjacent to aberrant methylation sites cannot well reflect the regulatory relationship between DNA methylation and gene transcription during the pathogenesis of arsenic-induced liver cancer, whereas a further analysis of the cis-regulatory elements and their trans-acting factors adjacent to DNA methylation can more precisely reflect the relationship between them. MYC and MAX (MYC associated factor X) were found to participating cell cycle through a bioinformatics analysis. Additionally, it was found that the hypomethylation of cis-regulatory sites in the MYC promoter region and the hypermethylation of cis-regulatory sites in the MAX promoter region result in the up-regulation of MYC mRNA expression and the down-regulation of MAX mRNA, which increased the hepatocyte carcinogenesis tendency.

Indexed as

DNA MethylationAmino Acid MotifsArsenicalsArsenic TrioxideBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCarcinogenesisCell LineCell Transformation, NeoplasticComputational BiologyGene Expression Regulation, NeoplasticHepatocytesHumansLiverLiver NeoplasmsOligonucleotide Array Sequence AnalysisOxidesArsenicalsArsenic TrioxideBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMAX protein, humanOxidesRNA, MessengerTranscription FactorsWnt Proteinsarsenic exposurecarcinogenesisDNA methylation

Identifiers

PMID26046465
PMCPMC4673281
OpenAlexW2149609127

What OpenQuestion holds

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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.