Evidence map›Paper›PMID 26350215›Full record

ArticleNucleic acids research2016

Epigenetic factor EPC1 is a master regulator of DNA damage response by interacting with E2F1 to silence death and activate metastasis-related gene signatures.

Yajie Wang, Vijay Alla, Deborah Goody, Shailendra K Gupta, Alf Spitschak, Olaf Wolkenhauer, Brigitte M Pützer, David Engelmann

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

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  10. Genes · 2022
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  13. Multiomics Integrative Analysis IdentifyingBioMed research international · 2022
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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

8 authors at 1 institution in 1 country.

Yajie WangInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
Vijay AllaInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
Deborah GoodyInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
Shailendra K GuptaDepartment of Systems Biology and Bioinformatics, University of Rostock, Rostock, Germany.
Alf SpitschakInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
Olaf WolkenhauerDepartment of Systems Biology and Bioinformatics, University of Rostock, Rostock, Germany.
Brigitte M PützerInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany brigitte.puetzer@med.uni-rostock.de.
David EngelmannInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
University of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription factor E2F1 is a key regulator of cell proliferation and apoptosis. Recently, it has been shown that aberrant E2F1 expression often detectable in advanced cancers contributes essentially to cancer cell propagation and characterizes the aggressive potential of a tumor. Conceptually, this requires a subset of malignant cells capable of evading apoptotic death through anticancer drugs. The molecular mechanism by which the pro-apoptotic activity of E2F1 is antagonized is widely unclear. Here we report a novel function for EPC1 (enhancer of polycomb homolog 1) in DNA damage protection. Depletion of EPC1 potentiates E2F1-mediated apoptosis in response to genotoxic treatment and abolishes tumor cell motility. We found that E2F1 directly binds to the EPC1 promoter and EPC1 vice versa physically interacts with bifunctional E2F1 to modulate its transcriptional activity in a target gene-specific manner. Remarkably, nuclear-colocalized EPC1 activates E2F1 to upregulate the expression of anti-apoptotic survival genes such as BCL-2 or Survivin/BIRC5 and inhibits death-inducing targets. The uncovered cooperativity between EPC1 and E2F1 triggers a metastasis-related gene signature in advanced cancers that predicts poor patient survival. These findings unveil a novel oncogenic function of EPC1 for inducing the switch into tumor progression-relevant gene expression that may help to set novel therapies.

Indexed as

DNA DamageGene Expression Regulation, NeoplasticGene SilencingApoptosisCell Line, TumorCell MovementChromosomal Proteins, Non-HistoneCluster AnalysisDrug Resistance, NeoplasmE2F1 Transcription FactorGene Expression ProfilingHumansNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsPolycomb-Group ProteinsChromosomal Proteins, Non-HistoneE2F1 Transcription FactorEPC1 protein, humanPolycomb-Group ProteinsRepressor Proteins

Identifiers

PMID26350215
PMCPMC4705687
OpenAlexW1590764257

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.