Evidence map›Paper›PMID 32034145›Full record

ArticleNature communications2020

C/EBPɑ is crucial determinant of epithelial maintenance by preventing epithelial-to-mesenchymal transition.

Ana Rita Lourenço, M Guy Roukens, Danielle Seinstra, Cynthia L Frederiks, Cornelieke E Pals, Stephin J Vervoort, Andreia S Margarido, Jacco van Rheenen, Paul J Coffer

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. 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
2.3field-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, 54 citations in OpenAlex.

  1. Article
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  3. HHIP's dynamic role in epithelial wound healing reveals a potential mechanism of COPD susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

9 authors at 3 institutions in 1 country.

Ana Rita LourençoCenter for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
M Guy Roukens *Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
Danielle Seinstra *Department of Molecular Pathology, Oncode Institute, Netherlands Cancer Institute, Plesmanlaan 121, Amsterdam, The Netherlands.
Cynthia L Frederiks *Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
Cornelieke E PalsCenter for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
Stephin J VervoortCenter for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
Andreia S MargaridoDepartment of Molecular Pathology, Oncode Institute, Netherlands Cancer Institute, Plesmanlaan 121, Amsterdam, The Netherlands.
Jacco van RheenenDepartment of Molecular Pathology, Oncode Institute, Netherlands Cancer Institute, Plesmanlaan 121, Amsterdam, The Netherlands.
Paul J CofferCenter for Molecular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands. pcoffer@umcutrecht.nl.
University Medical Center Utrecht · NLOncode Institute · NLThe Netherlands Cancer Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular signals such as TGF-β can induce epithelial-to-mesenchymal transition (EMT) in cancers of epithelial origin, promoting molecular and phenotypical changes resulting in pro-metastatic characteristics. We identified C/EBPα as one of the most TGF-β-mediated downregulated transcription factors in human mammary epithelial cells. C/EBPα expression prevents TGF-β-driven EMT by inhibiting expression of known EMT factors. Depletion of C/EBPα is sufficient to induce mesenchymal-like morphology and molecular features, while cells that had undergone TGF-β-induced EMT reverted to an epithelial-like state upon C/EBPα re-expression. In vivo, mice injected with C/EBPα-expressing breast tumor organoids display a dramatic reduction of metastatic lesions. Collectively, our results show that C/EBPα is required for maintaining epithelial homeostasis by repressing the expression of key mesenchymal markers, thereby preventing EMT-mediated tumorigenesis. These data suggest that C/EBPα is a master epithelial "gatekeeper" whose expression is required to prevent unwarranted mesenchymal transition, supporting an important role for EMT in mediating breast cancer metastasis.

Indexed as

AnimalsBreast NeoplasmsCCAAT-Enhancer-Binding ProteinsCells, CulturedEpithelial CellsEpithelial-Mesenchymal TransitionFemaleGene Expression RegulationHumansLung NeoplasmsMammary Glands, HumanMice, SCIDSmad3 ProteinTransforming Growth Factor betaXenograft Model Antitumor AssaysCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanSmad3 ProteinSMAD3 protein, humanTransforming Growth Factor beta

Identifiers

PMID32034145
PMCPMC7005738
OpenAlexW3005223335

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.