Evidence map›Paper›PMID 25008775›Full record

ArticleCell reports2014

A role for RUNX3 in inflammation-induced expression of IL23A in gastric epithelial cells.

Yit Teng Hor, Dominic Chih-Cheng Voon, Jason Kin Wai Koo, Huajing Wang, Wen Min Lau, Hassan Ashktorab, Shing Leng Chan, Yoshiaki Ito

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Inflammatory factors collaboratively linkFrontiers in immunology · 2025
    Review
  3. Article
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  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. RUNX3 is down-regulated in glioma by Myc-regulated miR-4295.Journal of cellular and molecular medicine · 2016
    Article
  15. Review
  16. Review
  17. NF-κB signaling pathway confers neuroblastoma cells migration and invasion ability via the regulation of CXCR4.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Article
  18. 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 at 2 institutions in 1 country.

Yit Teng HorCancer Stem Cells and Biology Programme, Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore; NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore 117456, Singapore.
Dominic Chih-Cheng VoonCancer Stem Cells and Biology Programme, Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore.
Jason Kin Wai KooCancer Stem Cells and Biology Programme, Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore.
Huajing WangCancer Stem Cells and Biology Programme, Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore.
Wen Min LauCancer Stem Cells and Biology Programme, Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore.
Hassan AshktorabCancer Center and Gastroenterology Division, Department of Medicine, Howard University Hospital, 2041 Georgia Avenue N.W., Washington, DC 20060, USA.
Shing Leng ChanCancer Stem Cells and Biology Programme, Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore.
Yoshiaki ItoCancer Stem Cells and Biology Programme, Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore. Electronic address: csiitoy@nus.edu.sg.
National University of Singapore · SGNational University Cancer Institute, Singapore · SG

Funding

PROTEOMICS CORE FACILITYG12MD007597 · NIMHD · HOWARD UNIVERSITY · PI SOUTHERLAND, WILLIAM M. · 2012 to 2018
$14.8M
NIMHD NIH HHS G12 MD007597
6 · The paper itself

Abstract

RUNX3 functions as a tumor suppressor in the gastric epithelium, where its inactivation is frequently observed during carcinogenesis. We identified IL23A as a RUNX3 target gene in gastric epithelial cells. This was confirmed in a series of in vitro analyses in gastric epithelial cell lines. In elucidating the underlying regulatory network, we uncovered a prominent role for the TNF-α/NF-κB pathway in activating IL23A transcription. Moreover, the activating effect of TNF-α was markedly augmented by the infection of Helicobacter pylori, the primary cause of human gastritis. Of note, H. pylori utilized the CagA/SHP2 pathway to activate IL23A, as well as the induction of the NOD1 pathway by iE-DAP. Importantly, RUNX3 synergized strongly with these physiologically relevant stimuli to induce IL23A. Lastly, we present evidence for the secretion of IL23A by gastric epithelial cells in a form that is distinct from canonical IL-23 (IL23A/IL12B).

Indexed as

Transcriptional ActivationAntigens, BacterialBacterial ProteinsCell LineCell Line, TumorCore Binding Factor Alpha 3 SubunitGastric MucosaHelicobacter pyloriHumansInflammationInterleukin-23 Subunit p19NF-kappa BNod1 Signaling Adaptor ProteinProtein Tyrosine Phosphatase, Non-Receptor Type 11Tumor Necrosis Factor-alphaAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriCore Binding Factor Alpha 3 SubunitIL23A protein, humanInterleukin-23 Subunit p19NF-kappa BNOD1 protein, humanNod1 Signaling Adaptor ProteinProtein Tyrosine Phosphatase, Non-Receptor Type 11Runx3 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID25008775
PMCPMC4307917
OpenAlexW2030620239

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.