Evidence map›Paper›PMID 29106391›Full record

ArticleOncogene2018

Aberrant GATA2 epigenetic dysregulation induces a GATA2/GATA6 switch in human gastric cancer.

S H Song, M S Jeon, J W Nam, J K Kang, Y J Lee, J Y Kang, H P Kim, S W Han, G H Kang, T Y Kim

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

24 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
  8. Review
  9. Article
  10. Role of the pioneer transcription factor GATA2 in health and disease.Journal of molecular medicine (Berlin, Germany) · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Hypoxia Alters Epigenetic andFrontiers in oncology · 2020
    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

10 authors at 2 institutions in 1 country.

S H SongCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
M S JeonCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
J W NamCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
J K KangCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
Y J LeeCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
J Y KangCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
H P KimCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
S W HanCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
G H KangLaboratory of Epigenetics, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
T Y KimCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
Seoul National University · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Six GATA transcription factors play important roles in eukaryotic development. Among these, GATA2, an essential factor for the hematopoietic cell lineage, exhibits low expression in human gastric tissues, whereas GATA6, which is crucial for gastrointestinal development and differentiation, is frequently amplified and/or overexpressed in human gastric cancer. Interestingly, we found that GATA6 was overexpressed in human gastric cancer cells only when GATA2 expression was completely absent, thereby showing an inverse correlation between GATA2 and GATA6. In gastric cancer cells that express high GATA6 levels, a GATA2 CpG island is hypermethylated, repressing expression in these cells. In contrast, GATA6 expression is undetectable in GATA2-overexpressing gastric cancer cells, which lack GATA2 DNA methylation. Furthermore, PRC2 complex-mediated transcriptional silencing of GATA6 was observed in the GATA2-overexpressing cells. We also show that the GATA2 and PRC2 complexes are enriched within the GATA6 locus, and that the recruitment of the PRC2 complex is impaired by disrupting GATA2 expression, resulting in GATA6 upregulation. In addition, ectopic GATA2 expression significantly downregulates GATA6 expression, suggesting GATA2 directly represses GATA6. Furthermore, GATA6 downregulation showed antitumor activity by inducing growth arrest. Finally, we show that aberrant GATA2 methylation occurs early during the multistep process of gastric carcinogenesis regardless of Helicobacter pylori infection. Taken together, GATA2 dysregulation by epigenetic modification is associated with unfavorable phenotypes in human gastric cancer cells by allowing GATA6 expression.

Indexed as

DNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticApoptosisBiomarkers, TumorCell ProliferationGATA2 Transcription FactorGATA6 Transcription FactorHumansPrognosisStomach NeoplasmsTumor Cells, CulturedBiomarkers, TumorGATA2 protein, humanGATA2 Transcription FactorGATA6 protein, humanGATA6 Transcription Factor

Identifiers

PMID29106391
OpenAlexW2768054523

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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.