Evidence map›Paper›PMID 28247944›Full record

ArticleCancer science2017

Ets1 and ESE1 reciprocally regulate expression of ZEB1/ZEB2, dependent on ERK1/2 activity, in breast cancer cells.

Nguyen Duy Sinh, Kaori Endo, Keiji Miyazawa, Masao Saitoh

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
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  4. Mutant p53 regulates reversible subtype plasticity in pancreatic cancer.Cellular and molecular life sciences : CMLS · 2025
    Article
  5. Article
  6. Roles of ZEB1 and ZEB2 in E-cadherin expression and cell aggressiveness in head and neck cancer.Genes to cells : devoted to molecular & cellular mechanisms · 2024
    Article
  7. Article
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  12. MAPKs in the early steps of senescence implemEMTation.Frontiers in cell and developmental biology · 2023
    Article
  13. Article
  14. Post-Translational Modification of ZEB Family Members in Cancer Progression.International journal of molecular sciences · 2022
    Review
  15. Review
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  17. Article
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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

4 authors at 1 institution in 1 country.

Nguyen Duy SinhDepartment of Biochemistry, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan.
Kaori EndoDepartment of Biochemistry, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan.
Keiji MiyazawaDepartment of Biochemistry, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan.
Masao SaitohDepartment of Biochemistry, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan.ORCID http://orcid.org/0000-0003-0793-1679
University of Yamanashi · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epithelial-mesenchymal transition (EMT) is a crucial morphological event that occurs during progression of epithelial tumors. We reported previously that levels of the δ-crystallin/E2-box factor 1 (δEF1) family proteins (Zinc finger E-box binding homeobox 1 [ZEB1]/δEF1 and ZEB2/ Smad-interacting protein 1), key regulators of the EMT, are positively correlated with EMT phenotypes and aggressiveness of breast cancer. Here, we show that Ets1 induces ZEB expression and activates the ZEB1 promoter, independently of its threonine 38 phosphorylation status. In the basal-like subtype of breast cancer cells, siRNAs targeting Ets1 repressed expression of ZEBs and partially restored their epithelial phenotypes and sensitivity to antitumor drugs. Epithelium-specific ETS transcription factor 1 (ESE1), a member of the Ets transcription factor family, was originally characterized as being expressed in an epithelial-restricted pattern, placing it within the epithelium-specific ETS subfamily. ESE1, highly expressed in the luminal subtype of breast cancer cells, was repressed by activation of the MEK-ERK pathway, resulting in induction of ZEBs through Ets1 upregulation. Conversely, Ets1, highly expressed in the basal-like subtype, was repressed by inactivation of MEK-ERK pathway, resulting in reduction of ZEBs through ESE1 upregulation. These findings suggest that ESE1 and Ets1, whose expressions are reciprocally regulated by the MEK-ERK pathway, define the EMT phenotype through controlling expression of ZEBs in each subtype of breast cancer cells.

Indexed as

Breast NeoplasmsCell Line, TumorDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleHomeodomain ProteinsHumansMAP Kinase Signaling SystemPhosphorylationPromoter Regions, GeneticProto-Oncogene Protein c-ets-1Proto-Oncogene Proteins c-etsRepressor ProteinsRNA, Small InterferingSignal TransductionTranscription FactorsDNA-Binding ProteinsELF3 protein, humanETS1 protein, humanHomeodomain ProteinsProto-Oncogene Protein c-ets-1Proto-Oncogene Proteins c-etsRepressor ProteinsRNA, Small InterferingTranscription FactorsZEB1 protein, humanZEB2 protein, humanZinc Finger E-box-Binding Homeobox 1Zinc Finger E-box Binding Homeobox 2EMTESE1Ets1signal transductionZEB

Identifiers

PMID28247944
PMCPMC5448599
OpenAlexW2593112691

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.