Evidence map›Paper›PMID 32190668›Full record

ArticleBioMed research international2020

Investigation of Potential Genetic Biomarkers and Molecular Mechanism of Ulcerative Colitis Utilizing Bioinformatics Analysis.

Jiaqi Zhang, Xue Wang, Lin Xu, Zedan Zhang, Fengyun Wang, Xudong Tang

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 43 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

6 authors at 1 institution in 1 country.

Jiaqi ZhangDepartment of Gastroenterology, Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing 100091, China.ORCID https://orcid.org/0000-0002-3143-5651
Xue WangExperimental Research Center of China Academy of Chinese Medical Sciences, Beijing 100700, China.
Lin XuDepartment of Gastroenterology, Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing 100091, China.ORCID https://orcid.org/0000-0003-2487-6528
Zedan ZhangDepartment of Gastroenterology, Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing 100091, China.
Fengyun WangDepartment of Gastroenterology, Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing 100091, China.ORCID https://orcid.org/0000-0002-4058-7905
Xudong TangChina Academy of Chinese Medical Sciences, Beijing 100700, China.ORCID https://orcid.org/0000-0003-0391-3895
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo reveal the molecular mechanisms of ulcerative colitis (UC) and provide potential biomarkers for UC gene therapy.

methodsWe downloaded the GSE87473 microarray dataset from the Gene Expression Omnibus (GEO) and identified the differentially expressed genes (DEGs) between UC samples and normal samples. Then, a module partition analysis was performed based on a weighted gene coexpression network analysis (WGCNA), followed by pathway and functional enrichment analyses. Furthermore, we investigated the hub genes. At last, data validation was performed to ensure the reliability of the hub genes.

resultsBetween the UC group and normal group, 988 DEGs were investigated. The DEGs were clustered into 5 modules using WGCNA. These DEGs were mainly enriched in functions such as the immune response, the inflammatory response, and chemotaxis, and they were mainly enriched in KEGG pathways such as the cytokine-cytokine receptor interaction, chemokine signaling pathway, and complement and coagulation cascades. The hub genes, including dual oxidase maturation factor 2 (DUOXA2), serum amyloid A (SAA) 1 and SAA2, TNFAIP3-interacting protein 3 (TNIP3), C-X-C motif chemokine (CXCL1), solute carrier family 6 member 14 (SLC6A14), and complement decay-accelerating factor (CD antigen CD55), were revealed as potential tissue biomarkers for UC diagnosis or treatment.

conclusionsThis study provides supportive evidence that DUOXA2, A-SAA, TNIP3, CXCL1, SLC6A14, and CD55 might be used as potential biomarkers for tissue biopsy of UC, especially SLC6A14 and DUOXA2, which may be new targets for UC gene therapy. Moreover, the DUOX2/DUOXA2 and CXCL1/CXCR2 pathways might play an important role in the progression of UC through the chemokine signaling pathway and inflammatory response.

Indexed as

Gene Expression ProfilingAdultAmino Acid Transport SystemsBiomarkers, TumorCD55 AntigensChemokine CXCL1Colitis, UlcerativeComputational BiologyDatabases, GeneticELAV-Like Protein 2FemaleGene Expression Regulation, NeoplasticGene Regulatory NetworksGenetic MarkersHumansIntracellular Signaling Peptides and ProteinsAmino Acid Transport SystemsBiomarkers, TumorCD55 AntigensChemokine CXCL1CXCL1 protein, humanDUOXA2 protein, humanELAVL2 protein, humanELAV-Like Protein 2Genetic MarkersIntracellular Signaling Peptides and ProteinsMembrane ProteinsSLC6A14 protein, humanTNIP3 protein, human

Identifiers

PMID32190668
PMCPMC7073481
OpenAlexW3010042726

What OpenQuestion holds

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LicenceCC BY
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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.