Evidence map›Paper›PMID 25896507›Full record

ArticleThe EMBO journal2015

Repression of SRF target genes is critical for Myc-dependent apoptosis of epithelial cells.

Katrin E Wiese, Heidi M Haikala, Björn von Eyss, Elmar Wolf, Cyril Esnault, Andreas Rosenwald, Richard Treisman, Juha Klefström, Martin Eilers

Abstract read
In one paragraph

Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Serum response factor is essential for endometrial function and prevention of inflammatory fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  16. MYC and AMPK-Save Energy or Die!Frontiers in cell and developmental biology · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 4 institutions in 3 countries.

Katrin E WieseBiocenter Theodor Boveri Institute University of Würzburg, Würzburg, Germany.
Heidi M HaikalaFaculty of Medicine, Cancer Cell Circuitry Laboratory, Translational Cancer Biology Research Program and Institute of Biomedicine Biomedicum Helsinki University of Helsinki, Helsinki, Finland.
Björn von EyssBiocenter Theodor Boveri Institute University of Würzburg, Würzburg, Germany.
Elmar WolfBiocenter Theodor Boveri Institute University of Würzburg, Würzburg, Germany.
Cyril EsnaultCancer Research UK London Research Institute Lincoln's Inn Fields Laboratories Transcription Laboratory, London, UK.
Andreas RosenwaldInstitute of Pathology University of Würzburg, Würzburg, Germany Comprehensive Cancer Center Mainfranken University of Würzburg, Würzburg, Germany.
Richard TreismanCancer Research UK London Research Institute Lincoln's Inn Fields Laboratories Transcription Laboratory, London, UK.
Juha KlefströmFaculty of Medicine, Cancer Cell Circuitry Laboratory, Translational Cancer Biology Research Program and Institute of Biomedicine Biomedicum Helsinki University of Helsinki, Helsinki, Finland.
Martin EilersBiocenter Theodor Boveri Institute University of Würzburg, Würzburg, Germany Comprehensive Cancer Center Mainfranken University of Würzburg, Würzburg, Germany martin.eilers@biozentrum.uni-wuerzburg.de.
University of Würzburg · DECancer Research UK · GBComprehensive Cancer Center Mainfranken · DEUniversity of Helsinki · FI

Funding

Cancer Research UK 15687
6 · The paper itself

Abstract

Oncogenic levels of Myc expression sensitize cells to multiple apoptotic stimuli, and this protects long-lived organisms from cancer development. How cells discriminate physiological from supraphysiological levels of Myc is largely unknown. Here, we show that induction of apoptosis by Myc in breast epithelial cells requires association of Myc with Miz1. Gene expression and ChIP-Sequencing experiments show that high levels of Myc invade target sites that lack consensus E-boxes in a complex with Miz1 and repress transcription. Myc/Miz1-repressed genes encode proteins involved in cell adhesion and migration and include several integrins. Promoters of repressed genes are enriched for binding sites of the serum-response factor (SRF). Restoring SRF activity antagonizes Myc repression of SRF target genes, attenuates Myc-induced apoptosis, and reverts a Myc-dependent decrease in Akt phosphorylation and activity, a well-characterized suppressor of Myc-induced apoptosis. We propose that high levels of Myc engage Miz1 in repressive DNA binding complexes and suppress an SRF-dependent transcriptional program that supports survival of epithelial cells.

Indexed as

ApoptosisCell AdhesionCell Line, TumorCell MovementEpithelial CellsFemaleHumansKruppel-Like Transcription FactorsMammary Glands, HumanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycSerum Response FactorTranscription, GeneticKruppel-Like Transcription FactorsMYC protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycSerum Response FactorZBTB17 protein, humanAktapoptosisMiz1Myc

Identifiers

PMID25896507
PMCPMC4474530
OpenAlexW1993360024

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.