Evidence map›Paper›PMID 32709847›Full record

ArticleCell death & disease2020

PRMT5 promotes cancer cell migration and invasion through the E2F pathway.

Wojciech Barczak, Li Jin, Simon Mark Carr, Shonagh Munro, Samuel Ward, Alexander Kanapin, Anastasia Samsonova, Nicholas B La Thangue

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  10. From DNA-Encoded Library Screening toJournal of medicinal chemistry · 2025
    Article
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  12. Targeting PRMT5 through PROTAC for the treatment of triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2024
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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 3 institutions in 2 countries.

Wojciech Barczak *Laboratory of Cancer Biology Department of Oncology, University of Oxford, Old Road Campus Research Building, Oxford, OX3 7DQ, UK.
Li Jin *Laboratory of Cancer Biology Department of Oncology, University of Oxford, Old Road Campus Research Building, Oxford, OX3 7DQ, UK.
Simon Mark CarrLaboratory of Cancer Biology Department of Oncology, University of Oxford, Old Road Campus Research Building, Oxford, OX3 7DQ, UK.
Shonagh MunroArgonaut Therapeutics Ltd Magdalen Centre, Oxford Science Park, Oxford, OX4 4GA, UK.
Samuel WardArgonaut Therapeutics Ltd Magdalen Centre, Oxford Science Park, Oxford, OX4 4GA, UK.
Alexander KanapinCentre for Genome Bioinformatics, St. Petersburg State University, St. Petersburg, 199034, Russia.
Anastasia SamsonovaCentre for Genome Bioinformatics, St. Petersburg State University, St. Petersburg, 199034, Russia.ORCID http://orcid.org/0000-0002-9353-9173
Nicholas B La ThangueLaboratory of Cancer Biology Department of Oncology, University of Oxford, Old Road Campus Research Building, Oxford, OX3 7DQ, UK. nick.lathangue@oncology.ox.ac.uk.
University of Oxford · GBSt Petersburg University · RUCancer Research UK · GB

Funding

Cancer Research UK 300/A13058
6 · The paper itself

Abstract

The pRb-E2F pathway is a critical point of regulation in the cell cycle and loss of control of the pathway is a hallmark of cancer. E2F1 is the major target through which pRb exerts its effects and arginine methylation by PRMT5 plays a key role in dictating E2F1 activity. Here we have explored the functional role of the PRMT5-E2F1 axis and highlight its influence on different aspects of cancer cell biology including viability, migration, invasion and adherence. Through a genome-wide expression analysis, we identified a distinct set of genes under the control of PRMT5 and E2F1, including some highly regulated genes, which influence cell migration, invasio and adherence through a PRMT5-dependent mechanism. Most significantly, a coincidence was apparent between the expression of PRMT5 and E2F1 in human tumours, and elevated levels of PRMT5 and E2F1 correlated with poor prognosis disease. Our results suggest a causal relationship between PRMT5 and E2F1 in driving the malignant phenotype and thereby highlight an important pathway for therapeutic intervention.

Indexed as

Cell MovementSignal TransductionCell Line, TumorCortactinDown-RegulationE2F1 Transcription FactorFocal AdhesionsGene Expression Regulation, NeoplasticGenome, HumanHumansNeoplasm InvasivenessNeoplasmsProtein-Arginine N-MethyltransferasesCortactinE2F1 Transcription FactorPRMT5 protein, humanProtein-Arginine N-Methyltransferases

Identifiers

PMID32709847
PMCPMC7382496
OpenAlexW3044725409

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.