Evidence map›Paper›PMID 31372511›Full record

ArticleCommunications biology2019

The role of GRHL2 and epigenetic remodeling in epithelial-mesenchymal plasticity in ovarian cancer cells.

Vin Yee Chung, Tuan Zea Tan, Jieru Ye, Rui-Lan Huang, Hung-Cheng Lai, Dennis Kappei, Heike Wollmann, Ernesto Guccione, Ruby Yun-Ju Huang

Abstract read
In one paragraph

Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
–field-weighted citation impact
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

61 citing papers in PubMed.

  1. Review
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  8. Defining the DNA Binding Specificity of GRHL2.bioRxiv : the preprint server for biology · 2026
    Article
  9. Article
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  11. Article
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  13. Article
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  15. Article
  16. Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024
    Review
  17. Review
  18. Article
  19. Cancer spreading patterns based on epithelial-mesenchymal plasticity.Frontiers in cell and developmental biology · 2024
    Article
  20. Identification of miR-6794-3p as a suppressor in pancreatic cancer metastasis.International journal of biological sciences · 2024
    Article

1 more citing papers are in PubMed but not listed here.

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

9 authors.

Vin Yee Chung1Cancer Science Institute of Singapore, National University of Singapore, Singapore, 117599 Singapore.ORCID 0000-0001-7011-2348
Tuan Zea Tan1Cancer Science Institute of Singapore, National University of Singapore, Singapore, 117599 Singapore.ORCID 0000-0001-6624-1593
Jieru Ye1Cancer Science Institute of Singapore, National University of Singapore, Singapore, 117599 Singapore.
Rui-Lan Huang2Department of Obstetrics and Gynecology, Shuang Ho Hospital, Taipei Medical University, 11031 Taipei, Taiwan.
Hung-Cheng Lai2Department of Obstetrics and Gynecology, Shuang Ho Hospital, Taipei Medical University, 11031 Taipei, Taiwan.
Dennis Kappei1Cancer Science Institute of Singapore, National University of Singapore, Singapore, 117599 Singapore.ORCID 0000-0002-3582-2253
Heike Wollmann4Institute of Molecular and Cell Biology, ASTAR, Singapore, 138673 Singapore.
Ernesto Guccione4Institute of Molecular and Cell Biology, ASTAR, Singapore, 138673 Singapore.
Ruby Yun-Ju Huang1Cancer Science Institute of Singapore, National University of Singapore, Singapore, 117599 Singapore.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells exhibit phenotypic plasticity during epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) involving intermediate states. To study genome-wide epigenetic remodeling associated with EMT plasticity, we integrate the analyses of DNA methylation, ChIP-sequencing of five histone marks (H3K4me1, H3K4me3, H3K27Ac, H3K27me3 and H3K9me3) and transcriptome profiling performed on ovarian cancer cells with different epithelial/mesenchymal states and on a knockdown model of EMT suppressor Grainyhead-like 2 (GRHL2). We have identified differentially methylated CpG sites associated with EMT, found at promoters of epithelial genes and GRHL2 binding sites. GRHL2 knockdown results in CpG methylation gain and nucleosomal remodeling (reduction in permissive marks H3K4me3 and H3K27ac; elevated repressive mark H3K27me3), resembling the changes observed across progressive EMT states. Epigenetic-modifying agents such as 5-azacitidine, GSK126 and mocetinostat further reveal cell state-dependent plasticity upon GRHL2 overexpression. Overall, we demonstrate that epithelial genes are subject to epigenetic control during intermediate phases of EMT/MET involving GRHL2.

Indexed as

Cell Line, TumorCpG IslandsDNA-Binding ProteinsDNA MethylationEpigenesis, GeneticEpithelial-Mesenchymal TransitionFemaleGene Knockdown TechniquesHistonesHumansOvarian NeoplasmsTranscription FactorsDNA-Binding ProteinsGRHL2 protein, humanHistonesTranscription FactorsDifferentiationEpigeneticsOvarian cancer

Identifiers

PMID31372511
PMCPMC6656769

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.