Evidence map›Paper›PMID 19935649›Full record

ArticleNature cell biology2009

The EMT-activator ZEB1 promotes tumorigenicity by repressing stemness-inhibiting microRNAs.

Ulrich Wellner, Jörg Schubert, Ulrike C Burk, Otto Schmalhofer, Feng Zhu, Annika Sonntag, Bettina Waldvogel, Corinne Vannier, Douglas Darling, Axel zur Hausen and 10 more

Abstract read
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In one paragraph

Article in Nature cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 998 papers.

0numbers the graph read from it
0cells of the map it votes in
998citing papers in PubMed
55.5field-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

998 citing papers in PubMed, 1,686 citations in OpenAlex.

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  8. Comprehensive analysis of the potential role of Ferroptosis-related genes in glioblastoma multiforme.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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938 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

20 authors at 6 institutions in 3 countries.

Ulrich WellnerDepartment of Visceral Surgery, University of Freiburg, 79106 Freiburg, Germany.
Jörg Schubert
Ulrike C Burk
Otto Schmalhofer
Feng Zhu
Annika Sonntag
Bettina Waldvogel
Corinne Vannier
Douglas Darling
Axel zur Hausen
Valerie G Brunton
Jennifer Morton
Owen Sansom
Julia Schüler
Marc P Stemmler
Christoph Herzberger
Ulrich Hopt
Tobias Keck
Simone Brabletz
Thomas Brabletz
University of Freiburg · DECancer Research UK Scotland Institute · GBEdinburgh Cancer Research · GBMax Planck Institute of Immunobiology and Epigenetics · DEOeko Institut · DEUniversity of Louisville · US

Funding

Cancer Research UK C157/A9148
6 · The paper itself

Abstract

Invasion and metastasis of carcinomas is promoted by the activation of the embryonic 'epithelial to mesenchymal transition' (EMT) program, which triggers cellular mobility and subsequent dissemination of tumour cells. We recently showed that the EMT-activator ZEB1 (zinc finger E-box binding homeobox 1) is a crucial promoter of metastasis and demonstrated that ZEB1 inhibits expression of the microRNA-200 (miR-200) family, whose members are strong inducers of epithelial differentiation. Here, we report that ZEB1 not only promotes tumour cell dissemination, but is also necessary for the tumour-initiating capacity of pancreatic and colorectal cancer cells. We show that ZEB1 represses expression of stemness-inhibiting miR-203 and that candidate targets of miR-200 family members are also stem cell factors, such as Sox2 and Klf4. Moreover, miR-200c, miR-203 and miR-183 cooperate to suppress expression of stem cell factors in cancer cells and mouse embryonic stem (ES) cells, as demonstrated for the polycomb repressor Bmi1. We propose that ZEB1 links EMT-activation and stemness-maintenance by suppressing stemness-inhibiting microRNAs (miRNAs) and thereby is a promoter of mobile, migrating cancer stem cells. Thus, targeting the ZEB1-miR-200 feedback loop might form the basis of a promising treatment for fatal tumours, such as pancreatic cancer.

Indexed as

Cell DifferentiationAnimalsBase SequenceCell Line, TumorEpithelial CellsGene Expression ProfilingGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMesenchymal Stem CellsMiceMice, NudeMicroRNAsHomeodomain ProteinsKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsTranscription FactorsZEB1 protein, humanZEB1 protein, mouseZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID19935649
OpenAlexW2147807172

What OpenQuestion holds

Textmetadata
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.