Evidence map›Paper›PMID 32692442›Full record

ArticleThe EMBO journal2020

Genome-wide cooperation of EMT transcription factor ZEB1 with YAP and AP-1 in breast cancer.

Nora Feldker, Fulvia Ferrazzi, Harald Schuhwerk, Sebastian A Widholz, Kerstin Guenther, Isabell Frisch, Kathrin Jakob, Julia Kleemann, Dania Riegel, Ulrike Bönisch and 6 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
13.0field-weighted citation impact, top 1% 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

118 citing papers in PubMed, 160 citations in OpenAlex.

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  18. INHBA: A Protein-coding Gene Closely Related to Tumour Diseases.Current topics in medicinal chemistry · 2026
    Review
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58 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

16 authors at 3 institutions in 1 country.

Nora Feldker *Department of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Fulvia Ferrazzi *Institute of Human Genetics, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.ORCID 0000-0003-4011-4638
Harald SchuhwerkDepartment of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Sebastian A WidholzDepartment of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.ORCID 0000-0002-4566-2986
Kerstin GuentherDepartment of Visceral Surgery, Faculty of Biology, University of Freiburg, Freiburg, Germany.
Isabell FrischDepartment of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Kathrin JakobDepartment of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Julia KleemannDepartment of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Dania RiegelRegensburg Center for Interventional Immunology (RCI), University Regensburg and University Medical Center, Regensburg, Germany.
Ulrike BönischMax Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Sören LukassenInstitute of Human Genetics, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.ORCID 0000-0001-7045-6327
Rebecca L EcclesDepartment of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Christian SchmidlRegensburg Center for Interventional Immunology (RCI), University Regensburg and University Medical Center, Regensburg, Germany.
Marc P StemmlerDepartment of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.ORCID 0000-0002-7866-3686
Thomas BrabletzDepartment of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.ORCID 0000-0003-2983-9048
Simone BrabletzDepartment of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.ORCID 0000-0003-0936-1526
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEMax Planck Institute of Immunobiology and Epigenetics · DEUniversity of Freiburg · DE

Funding

Deutsche Forschungsgemeinschaft (DFG) BR 1399/10-1Deutsche Forschungsgemeinschaft (DFG) BR 1399/13-1Deutsche Forschungsgemeinschaft (DFG) BR 1399/9-1Deutsche Forschungsgemeinschaft (DFG) BR 4145/1-1Deutsche Forschungsgemeinschaft (DFG) BR 4145/2-1Deutsche Forschungsgemeinschaft (DFG) SFB992/C06Interdisziplin-äres Zentrum für Klinische Forschung, Universitätsklinikum Erlangen F4-46Universität Erlangen, Medizinische Fakultät, ELAN 29624020
6 · The paper itself

Abstract

Invasion, metastasis and therapy resistance are the major cause of cancer-associated deaths, and the EMT-inducing transcription factor ZEB1 is a crucial stimulator of these processes. While work on ZEB1 has mainly focused on its role as a transcriptional repressor, it can also act as a transcriptional activator. To further understand these two modes of action, we performed a genome-wide ZEB1 binding study in triple-negative breast cancer cells. We identified ZEB1 as a novel interactor of the AP-1 factors FOSL1 and JUN and show that, together with the Hippo pathway effector YAP, they form a transactivation complex, predominantly activating tumour-promoting genes, thereby synergising with its function as a repressor of epithelial genes. High expression of ZEB1, YAP, FOSL1 and JUN marks the aggressive claudin-low subtype of breast cancer, indicating the translational relevance of our findings. Thus, our results link critical tumour-promoting transcription factors: ZEB1, AP-1 and Hippo pathway factors. Disturbing their molecular interaction may provide a promising treatment option for aggressive cancer types.

Indexed as

Epithelial-Mesenchymal TransitionGenome, HumanAdaptor Proteins, Signal TransducingBreast NeoplasmsCell Line, TumorFemaleFos-Related Antigen 1HumansProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junTranscription Factor AP-1Transcription FactorsYAP-Signaling ProteinsZinc Finger E-box-Binding Homeobox 1Adaptor Proteins, Signal TransducingFos-Related Antigen 1JUN protein, humanProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junTranscription Factor AP-1Transcription FactorsYAP1 protein, humanYAP-Signaling ProteinsZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1AP-1breast cancerepithelial to mesenchymal transitionZEB1

Identifiers

PMID32692442
PMCPMC7459422
OpenAlexW3044823707

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.