Evidence map›Paper›PMID 32960383›Full record

ArticleDigestive diseases and sciences2021

Identification of Significant Genes and Pathways in Acute Pancreatitis via Bioinformatical Analysis.

Ran Ji, Ying Chen, Weiwei Chen, Yuming Wang, Fangchen Gong, Shunwei Huang, Rongli Xie, Ming Zhong, Zhaojun Liu, Zhitao Yang and 3 more

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Claudin-4: A New Molecular Target for Epithelial Cancer Therapy.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Claudin and pancreatic cancer.Frontiers in oncology · 2023
    Review
  8. Article
  9. 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

13 authors at 1 institution in 1 country.

Ran Ji *Ruijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Ying Chen *Ruijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Weiwei ChenRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Yuming WangRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Fangchen GongRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Shunwei HuangRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Rongli XieRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Ming ZhongRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Zhaojun LiuRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Zhitao YangRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Jian FeiRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Enqiang MaoRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China.
Erzhen ChenRuijin Hospital, No. 197 Ruijin 2nd Road, Shanghai, 200001, China. rjchenerzhen@163.com.
Ruijin Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsAcute pancreatitis (AP) is one of the common acute abdominal diseases with complicated pathogenesis. The purpose of this study is to identify the differentially expressed genes (DEGs) in the pancreas and underlying mechanisms.

methodsGene expression profiles of GSE109227 and GSE65146 were available from GEO database. Then, an integrated analysis of these genes was performed, including gene ontology (GO) and KEGG pathway enrichment analysis, protein-protein interaction (PPI) network construction, core gene correlation analysis, transcription factors (TFs) prediction, and expression level evaluation in human organs.

resultsA total number of 92 differential expressed genes were screened from the datasets, including 81 up-regulated genes and 11 down-regulated genes. The up-regulated genes were mainly enriched in the biological process, such as sarcomere organization, actin cytoskeleton organization, tumor necrosis factor biosynthetic process, response to cytokine, cell-cell adhesion, and the cell migration, and also involved in some signaling pathways, including leukocyte transendothelial migration, proteoglycans in cancer, thyroid cancer, cell adhesion, tight junction, bladder cancer, amoebiasis, glycerolipid metabolism, and VEGF signaling pathway, while down-regulated genes were significantly enriched in the endoplasmic reticulum unfolded protein response, the oxidation-reduction, and no significant signaling pathways. CDH1 and CLDN4 were identified as core genes by PPI network analysis with MCODE plug-in, as well as GO and KEGG re-enrichment. For validation in Gene Expression Profiling Interactive Analysis (GEPIA), CDH1 and CLDN4 were interacting with each other and regulated by the predictive common TFs FOXP3 or USF2. The two core genes and USF2 were expressed in varied human organs including the pancreas, while FOXP3 was not detected in the normal human pancreatic tissues.

conclusionsThis study implied that core gene CDH1 and CLDN4, which might be regulated by FOXP3 or USF2, played a significant role in acute pancreatitis. They could be potential diagnostic and therapeutic targets for AP patients.

Indexed as

Antigens, CDCadherinsClaudin-4Computational BiologyGene Expression ProfilingGene OntologyGene Regulatory NetworksHumansPancreatitisProtein Interaction MappingSignal TransductionAntigens, CDCadherinsCDH1 protein, humanClaudin-4CLDN4 protein, humanAcute pancreatitisBioinformatical analysisDifferentially expressed geneMicroarray

Identifiers

PMID32960383
OpenAlexW3086999381

What OpenQuestion holds

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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.