Evidence map›Paper›PMID 24582497›Full record

ArticleMolecular cell2014

The breast cancer oncogene EMSY represses transcription of antimetastatic microRNA miR-31.

Emmanuelle Viré, Christina Curtis, Veronica Davalos, Anna Git, Samuel Robson, Alberto Villanueva, August Vidal, Isaia Barbieri, Samuel Aparicio, Manel Esteller and 2 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Prognostic role of microRNA-31 in various cancers: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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  10. On the NF-Y regulome as in ENCODE (2019).PLoS computational biology · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 6 institutions in 3 countries.

Emmanuelle ViréGurdon Institute and Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.
Christina CurtisDepartment of Oncology and Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, CB2 0RE, UK.
Veronica DavalosCancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL), Barcelona 08907, Spain.
Anna GitDepartment of Oncology and Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, CB2 0RE, UK.
Samuel RobsonGurdon Institute and Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.
Alberto VillanuevaCancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL), Barcelona 08907, Spain.
August VidalDepartment of Pathological Anatomy, Bellvitge University Hospital, Bellvitge Biomedical Research Institute (IDIBELL), Barcelona 08907, Spain.
Isaia Barbieri
Samuel AparicioDepartment of Molecular Oncology, British Columbia Cancer Agency, 675 West 10(th) Avenue, V5Z 1L3 Vancouver, Canada.
Manel EstellerCancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL), Barcelona 08907, Spain.
Carlos CaldasDepartment of Oncology and Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, CB2 0RE, UK; Cambridge Breast Unit, Addenbrooke's Hospital, Cambridge University Hospital, NHS Foundation Trust and NIHR Cambridge Biomedical Research Centre, Cambridge CB2 2QQ, UK; Cambridge Experimental Cancer Medicine Centre (ECMC), Cambridge CB2 0RE, UK.
Tony KouzaridesGurdon Institute and Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK. Electronic address: t.kouzarides@gurdon.cam.ac.uk.
Institut d'Investigació Biomédica de Bellvitge · ESCancer Research UK · GBUniversity of Cambridge · GBWellcome/Cancer Research UK Gurdon Institute · GBBC Cancer Agency · CACambridge University Hospitals NHS Foundation Trust · GB

Funding

Cancer Research UK 10827Cancer Research UK 16942Cancer Research UK 17001Wellcome Trust 092096
6 · The paper itself

Abstract

Amplification of the EMSY gene in sporadic breast and ovarian cancers is a poor prognostic indicator. Although EMSY has been linked to transcriptional silencing, its mechanism of action is unknown. Here, we report that EMSY acts as an oncogene, causing the transformation of cells in vitro and potentiating tumor formation and metastatic features in vivo. We identify an inverse correlation between EMSY amplification and miR-31 expression, an antimetastatic microRNA, in the METABRIC cohort of human breast samples. Re-expression of miR-31 profoundly reduced cell migration, invasion, and colony-formation abilities of cells overexpressing EMSY or haboring EMSY amplification. We show that EMSY is recruited to the miR-31 promoter by the DNA binding factor ETS-1, and it represses miR-31 transcription by delivering the H3K4me3 demethylase JARID1b/PLU-1/KDM5B. Altogether, these results suggest a pathway underlying the role of EMSY in breast cancer and uncover potential diagnostic and therapeutic targets in sporadic breast cancer.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBase SequenceBreast NeoplasmsCell MovementCohort StudiesFemaleGene SilencingHumansMCF-7 CellsMiceMice, NudeMicroRNAsMolecular Sequence DataNeoplasm InvasivenessNeoplasm MetastasisEMSY protein, humanMicroRNAsMIRN31 microRNA, humanNeoplasm ProteinsNuclear ProteinsRepressor ProteinsRNA, Small Interfering

Identifiers

PMID24582497
PMCPMC3988886
OpenAlexW1986571428

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.