Evidence map›Paper›PMID 27461468›Full record

ArticleHuman genomics2016

The up-regulation of Myb may help mediate EGCG inhibition effect on mouse lung adenocarcinoma.

Hong Zhou, Joseph Manthey, Ekaterina Lioutikova, William Yang, Kenji Yoshigoe, Mary Qu Yang, Hong Wang

Open access · goldAbstract read
In one paragraph

Article in Human genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 15 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

7 authors at 4 institutions in 1 country.

Hong ZhouDepartment of Mathematical Science, School of Health and Natural Sciences, University of Saint Joseph, 1678 Asylum Avenue, West Hartford, CT, 06117, USA. hzhou@usj.edu.
Joseph MantheyDepartment of Mathematical Science, School of Health and Natural Sciences, University of Saint Joseph, 1678 Asylum Avenue, West Hartford, CT, 06117, USA.
Ekaterina LioutikovaDepartment of Mathematical Science, School of Health and Natural Sciences, University of Saint Joseph, 1678 Asylum Avenue, West Hartford, CT, 06117, USA.
William YangJoint Bioinformatics Ph.D. Program, University of Arkansas at Little Rock and University of Arkansas for Medical Sciences, 2801 S. University Avenue, Little Rock, AR, 72204, USA.
Kenji YoshigoeJoint Bioinformatics Ph.D. Program, University of Arkansas at Little Rock and University of Arkansas for Medical Sciences, 2801 S. University Avenue, Little Rock, AR, 72204, USA.
Mary Qu YangJoint Bioinformatics Ph.D. Program, University of Arkansas at Little Rock and University of Arkansas for Medical Sciences, 2801 S. University Avenue, Little Rock, AR, 72204, USA. mqyang@ualr.edu.
Hong WangSusan L. Cullman Laboratory for Cancer Research, Department of Chemical Biology and Centre for Cancer Prevention Research, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, 164 Frelinghuysen Road, Piscataway, NJ, 08854, USA.
University of Saint Joseph · USUniversity of Arkansas at Little Rock · USRutgers, The State University of New Jersey · USUniversity of Arkansas for Medical Sciences · US

Funding

Developing integrative approaches for identifying disease-causing genes and dysfunctional networksR15GM114739 · NIGMS · UNIVERSITY OF ARKANSAS AT LITTLE ROCK · PI YANG, MARY · 2015 to 2015
$374k
NIGMS NIH HHS R15 GM114739
6 · The paper itself

Abstract

backgroundGreen tea polyphenol epigallocatechin-3-gallate (EGCG) has been demonstrated to inhibit cancer in experimental studies through its antioxidant activity and modulations on cellular functions by binding specific proteins. By means of computational analysis and functional genomic approaches, we previously identified a set of protein coding genes and microRNAs whose expressions were significantly modulated in response to the EGCG treatment in tobacco carcinogen-induced lung adenocarcinoma in A/J mice. However, to what degree these genes are involved in the cancer inhibition of EGCG remains unclear.

resultsIn this study, we further employed statistical methods and literature research to analyze these data in combination with The Cancer Genome Atlas (TCGA) lung adenocarcinoma datasets for additional data mining. Under the assumption that, if a gene mediates EGCG's cancer inhibition, its expression level change caused by EGCG should be opposite to what occurred in the carcinogenesis, we identified Myb and Peg3 as the primary putative genes involved in the cancer inhibitory activity. Further analysis suggested that the regulation of Myb could be mediated through an EGCG-upregulated microRNA, miR-449c-5p.

conclusionsAlthough the actions of EGCG involve multiple targets/pathways, further analysis by mining the existing genomic datasets revealed that the upregulations of Myb and Peg3 are likely the key anti-cancer events of EGCG in vivo.

Indexed as

AdenocarcinomaAnimalsAntioxidantsCatechinGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksKruppel-Like Transcription FactorsLungLung NeoplasmsMice, Inbred StrainsMicroRNAsProto-Oncogene Proteins c-mybUp-RegulationAntioxidantsCatechinepigallocatechin gallateKruppel-Like Transcription FactorsMicroRNAsPeg3 protein, mouseProto-Oncogene Proteins c-myb

Identifiers

PMID27461468
PMCPMC4965723
OpenAlexW2483781252

What OpenQuestion holds

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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.