Evidence map›Paper›PMID 29317486›Full record

ArticleGenes & development2017

Mutual dependence of the MRTF-SRF and YAP-TEAD pathways in cancer-associated fibroblasts is indirect and mediated by cytoskeletal dynamics.

Charles T Foster, Francesco Gualdrini, Richard Treisman

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
–field-weighted citation impact
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

137 citing papers in PubMed, 203 citations in OpenAlex.

  1. Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026
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  14. Tumors and their microenvironments: Learning from pediatric brain pathologies.Biochimica et biophysica acta. Reviews on cancer · 2025
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  18. Cancer-associated fibroblasts in carcinogenesis.Journal of translational medicine · 2025
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77 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

3 authors at 1 institution in 1 country.

Charles T FosterSignalling and Transcription Group, Francis Crick Institute, London NW1 1AT, United Kingdom.
Francesco GualdriniSignalling and Transcription Group, Francis Crick Institute, London NW1 1AT, United Kingdom.
Richard TreismanSignalling and Transcription Group, Francis Crick Institute, London NW1 1AT, United Kingdom.ORCID 0000-0002-9658-0067
The Francis Crick Institute · GB

Funding

Cancer Research UK FC001-190European Research Council 268690Medical Research Council FC001-190Wellcome Trust FC001-190Wellcome Trust FC001190
6 · The paper itself

Abstract

Both the MRTF-SRF and the YAP-TEAD transcriptional regulatory networks respond to extracellular signals and mechanical stimuli. We show that the MRTF-SRF pathway is activated in cancer-associated fibroblasts (CAFs). The MRTFs are required in addition to the YAP pathway for CAF contractile and proinvasive properties. We compared MRTF-SRF and YAP-TEAD target gene sets and identified genes directly regulated by one pathway, the other, or both. Nevertheless, the two pathways exhibit mutual dependence. In CAFs, expression of direct MRTF-SRF genomic targets is also dependent on YAP-TEAD activity, and, conversely, YAP-TEAD target gene expression is also dependent on MRTF-SRF signaling. In normal fibroblasts, expression of activated MRTF derivatives activates YAP, while activated YAP derivatives activate MRTF. Cross-talk between the pathways requires recruitment of MRTF and YAP to DNA via their respective DNA-binding partners (SRF and TEAD) and is therefore indirect, arising as a consequence of activation of their target genes. In both CAFs and normal fibroblasts, we found that YAP-TEAD activity is sensitive to MRTF-SRF-induced contractility, while MRTF-SRF signaling responds to YAP-TEAD-dependent TGFβ signaling. Thus, the MRF-SRF and YAP-TEAD pathways interact indirectly through their ability to control cytoskeletal dynamics.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCancer-Associated FibroblastsCell Cycle ProteinsCell Line, TumorCytoskeletonDNA-Binding ProteinsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMammary Neoplasms, AnimalMicePhosphoproteinsSignal TransductionTEA Domain Transcription FactorsAdaptor Proteins, Signal TransducingCell Cycle ProteinsDNA-Binding ProteinsMRTFA protein, humanMrtfa protein, mousePhosphoproteinsTead1 protein, mouseTEA Domain Transcription FactorsTrans-ActivatorsTranscription FactorsTransforming Growth Factor beta1Yap1 protein, mouseYAP-Signaling Proteinscancer-associated fibroblastmechanotransductionMRTFSRFTEADtranscriptionYAP

Identifiers

PMID29317486
PMCPMC5795783
OpenAlexW2783271194

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.