Evidence map›Paper›PMID 30285803›Full record

ArticleBreast cancer research : BCR2018

Foxf2 plays a dual role during transforming growth factor beta-induced epithelial to mesenchymal transition by promoting apoptosis yet enabling cell junction dissolution and migration.

Nathalie Meyer-Schaller, Chantal Heck, Stefanie Tiede, Mahmut Yilmaz, Gerhard Christofori

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Review
  5. The Role of the Fox Gene in Breast Cancer Progression.International journal of molecular sciences · 2025
    Review
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  20. Effects of VEGFR1Journal of cancer research and clinical oncology · 2019
    Article
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

5 authors at 2 institutions in 2 countries.

Nathalie Meyer-SchallerDepartment of Biomedicine, University of Basel, Mattenstrasse 28, 4058, Basel, Switzerland.
Chantal HeckDepartment of Biomedicine, University of Basel, Mattenstrasse 28, 4058, Basel, Switzerland.
Stefanie TiedeDepartment of Biomedicine, University of Basel, Mattenstrasse 28, 4058, Basel, Switzerland.
Mahmut YilmazDepartment of Biomedicine, University of Basel, Mattenstrasse 28, 4058, Basel, Switzerland.
Gerhard ChristoforiDepartment of Biomedicine, University of Basel, Mattenstrasse 28, 4058, Basel, Switzerland. gerhard.christofori@unibas.ch.ORCID 0000-0002-8696-9896
University of Basel · CHRoche (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe most life-threatening step during malignant tumor progression is reached when cancer cells leave the primary tumor mass and seed metastasis in distant organs. To infiltrate the surrounding tissue and disseminate throughout the body, single motile tumor cells leave the tumor mass by breaking down cell-cell contacts in a process called epithelial to mesenchymal transition (EMT). An EMT is a complex molecular and cellular program enabling epithelial cells to abandon their differentiated phenotype, including cell-cell adhesion and cell polarity, and to acquire mesenchymal features and invasive properties.

methodsWe employed gene expression profiling and functional experiments to study transcriptional control of transforming growth factor (TGF)β-induced EMT in normal murine mammary gland epithelial (NMuMG) cells.

resultsWe identified that expression of the transcription factor forkhead box protein F2 (Foxf2) is upregulated during the EMT process. Although it is not required to gain mesenchymal markers, Foxf2 is essential for the disruption of cell junctions and the downregulation of epithelial markers in NMuMG cells treated with TGFβ. Foxf2 is critical for the downregulation of E-cadherin by promoting the expression of the transcriptional repressors of E-cadherin, Zeb1 and Zeb2, while repressing expression of the epithelial maintenance factor Id2 and miRNA 200 family members. Moreover, Foxf2 is required for TGFβ-mediated apoptosis during EMT by the transcriptional activation of the proapoptotic BH3-only protein Noxa and by the negative regulation of epidermal growth factor receptor (EGFR)-mediated survival signaling through direct repression of its ligands betacellulin and amphiregulin. The dual function of Foxf2 during EMT is underscored by the finding that high Foxf2 expression correlates with good prognosis in patients with early noninvasive stages of breast cancer, but with poor prognosis in advanced breast cancer.

conclusionsOur data identify the transcription factor Foxf2 as one of the important regulators of EMT, displaying a dual function in promoting tumor cell apoptosis as well as tumor cell migration.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBreast NeoplasmsCell LineCell MovementEpithelial CellsEpithelial-Mesenchymal TransitionFemaleForkhead Transcription FactorsHumansIntercellular JunctionsMCF-7 CellsMiceTransforming Growth Factor betaForkhead Transcription FactorsTransforming Growth Factor betaApoptosisBreast cancerCell migrationE-cadherinEGFREMTFoxf2Noxa

Identifiers

PMID30285803
PMCPMC6167826
OpenAlexW2893130780

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.