Evidence map›Paper›PMID 28412966›Full record

ArticleBiology direct2017

TFAP2A is a component of the ZEB1/2 network that regulates TGFB1-induced epithelial to mesenchymal transition.

Yoana Dimitrova, Andreas J Gruber, Nitish Mittal, Souvik Ghosh, Beatrice Dimitriades, Daniel Mathow, William Aaron Grandy, Gerhard Christofori, Mihaela Zavolan

Open access · goldAbstract read
In one paragraph

Article in Biology direct, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

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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 2 institutions in 2 countries.

Yoana DimitrovaBiozentrum, University of Basel, Klingelbergstrasse 50-70, CH-4056, Basel, Switzerland.
Andreas J GruberBiozentrum, University of Basel, Klingelbergstrasse 50-70, CH-4056, Basel, Switzerland.
Nitish MittalBiozentrum, University of Basel, Klingelbergstrasse 50-70, CH-4056, Basel, Switzerland.
Souvik GhoshBiozentrum, University of Basel, Klingelbergstrasse 50-70, CH-4056, Basel, Switzerland.
Beatrice DimitriadesBiozentrum, University of Basel, Klingelbergstrasse 50-70, CH-4056, Basel, Switzerland.
Daniel MathowDepartment of Cellular and Molecular Pathology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
William Aaron GrandyBiozentrum, University of Basel, Klingelbergstrasse 50-70, CH-4056, Basel, Switzerland.
Gerhard ChristoforiDepartment of Biomedicine, University of Basel, Mattenstrasse 28, CH-4058, Basel, Switzerland.
Mihaela ZavolanBiozentrum, University of Basel, Klingelbergstrasse 50-70, CH-4056, Basel, Switzerland. mihaela.zavolan@unibas.ch.ORCID 0000-0002-8832-2041
University of Basel · CHGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe transition between epithelial and mesenchymal phenotypes (EMT) occurs in a variety of contexts. It is critical for mammalian development and it is also involved in tumor initiation and progression. Master transcription factor (TF) regulators of this process are conserved between mouse and human.

methodsFrom a computational analysis of a variety of high-throughput sequencing data sets we initially inferred that TFAP2A is connected to the core EMT network in both species. We then analysed publicly available human breast cancer data for TFAP2A expression and also studied the expression (by mRNA sequencing), activity (by monitoring the expression of its predicted targets), and binding (by electrophoretic mobility shift assay and chromatin immunoprecipitation) of this factor in a mouse mammary gland EMT model system (NMuMG) cell line.

resultsWe found that upon induction of EMT, the activity of TFAP2A, reflected in the expression level of its predicted targets, is up-regulated in a variety of systems, both murine and human, while TFAP2A's expression is increased in more "stem-like" cancers. We provide strong evidence for the direct interaction between the TFAP2A TF and the ZEB2 promoter and we demonstrate that this interaction affects ZEB2 expression. Overexpression of TFAP2A from an exogenous construct perturbs EMT, however, in a manner similar to the downregulation of endogenous TFAP2A that takes place during EMT.

conclusionsOur study reveals that TFAP2A is a conserved component of the core network that regulates EMT, acting as a repressor of many genes, including ZEB2. REVIEWERS: This article has been reviewed by Dr. Martijn Huynen and Dr. Nicola Aceto.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell LineEpithelial-Mesenchymal TransitionFemaleHomeodomain ProteinsHumansMammary Glands, AnimalMiceRepressor ProteinsTranscription Factor AP-2Transforming Growth Factor beta1Zinc Finger E-box-Binding Homeobox 1Zinc Finger E-box Binding Homeobox 2Homeodomain ProteinsRepressor ProteinsTfap2a protein, mouseTgfb1 protein, mouseTranscription Factor AP-2Transforming Growth Factor beta1ZEB1 protein, mouseZEB2 protein, mouseZinc Finger E-box-Binding Homeobox 1Zinc Finger E-box Binding Homeobox 2EMTEpithelial-to-mesenchymal transitionNMuMGTFAP2ATGFb1Transcription regulatory networkZEB2

Identifiers

PMID28412966
PMCPMC5392957
OpenAlexW2606972010

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.