Evidence map›Paper›PMID 36170835›Full record

ArticleCell reports2022

FOXA1 regulates alternative splicing in prostate cancer.

Marco Del Giudice, John G Foster, Serena Peirone, Alberto Rissone, Livia Caizzi, Federica Gaudino, Caterina Parlato, Francesca Anselmi, Rebecca Arkell, Simonetta Guarrera and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-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

27 citing papers in PubMed, 33 citations in OpenAlex.

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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

14 authors at 5 institutions in 2 countries.

Marco Del GiudiceItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Candiolo Cancer Institute, FPO-IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy.
John G FosterCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Cancer Research UK Barts Centre, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Serena PeironeItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Department of Biosciences, Università degli Studi di Milano, Via Celoria 26, 20133 Milan, Italy.
Alberto RissoneItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Candiolo Cancer Institute, FPO-IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy.
Livia CaizziItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Candiolo Cancer Institute, FPO-IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy.
Federica GaudinoItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Candiolo Cancer Institute, FPO-IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy.
Caterina ParlatoItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Candiolo Cancer Institute, FPO-IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy.
Francesca AnselmiItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Department of Life Science and System Biology, Università degli Studi di Torino, via Accademia Albertina 13, 10123 Turin, Italy.
Rebecca ArkellCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Cancer Research UK Barts Centre, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Simonetta GuarreraItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Candiolo Cancer Institute, FPO-IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy.
Salvatore OlivieroItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Department of Life Science and System Biology, Università degli Studi di Torino, via Accademia Albertina 13, 10123 Turin, Italy.
Giuseppe BassoItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Candiolo Cancer Institute, FPO-IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy.
Prabhakar RajanCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Cancer Research UK Barts Centre, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK; Division of Surgery and Interventional Science, University College London, Charles Bell House, 3 Road Floor, 43-45 Foley Street, London W1W 7TS, UK; The Alan Turing Institute, British Library, 96 Euston Road, London NW1 2DB, UK; Department of Urology, Barts Health NHS Trust, the Royal London Hospital, Whitechapel Road, London E1 1BB, UK; Department of Uro-oncology, University College London NHS Foundation Trust, 47 Wimpole Street, London W1G 8SE, UK. Electronic address: p.rajan@qmul.ac.uk.
Matteo CeredaItalian Institute for Genomic Medicine, c/o IRCCS, Str. Prov. le 142, km 3.95, 10060 Candiolo (TO), Italy; Department of Biosciences, Università degli Studi di Milano, Via Celoria 26, 20133 Milan, Italy. Electronic address: matteo.cereda1@unimi.it.
Istituti di Ricovero e Cura a Carattere Scientifico · ITItalian institute for Genomic Medicine · ITQueen Mary University of London · GBCancer Research UK · GBCandiolo Cancer Institute · IT

Funding

Cancer Research UK 15339Cancer Research UK C19198/A15339
6 · The paper itself

Abstract

Dysregulation of alternative splicing in prostate cancer is linked to transcriptional programs activated by AR, ERG, FOXA1, and MYC. Here, we show that FOXA1 functions as the primary orchestrator of alternative splicing dysregulation across 500 primary and metastatic prostate cancer transcriptomes. We demonstrate that FOXA1 binds to the regulatory regions of splicing-related genes, including HNRNPK and SRSF1. By controlling trans-acting factor expression, FOXA1 exploits an "exon definition" mechanism calibrating alternative splicing toward dominant isoform production. This regulation especially impacts splicing factors themselves and leads to a reduction of nonsense-mediated decay (NMD)-targeted isoforms. Inclusion of the NMD-determinant FLNA exon 30 by FOXA1-controlled oncogene SRSF1 promotes cell growth in vitro and predicts disease recurrence. Overall, we report a role for FOXA1 in rewiring the alternative splicing landscape in prostate cancer through a cascade of events from chromatin access, to splicing factor regulation, and, finally, to alternative splicing of exons influencing patient survival.

Indexed as

Alternative SplicingProstatic NeoplasmsChromatinHepatocyte Nuclear Factor 3-alphaHumansMaleNeoplasm Recurrence, LocalRNA Splicing FactorsSerine-Arginine Splicing FactorsTrans-ActivatorsChromatinFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaRNA Splicing FactorsSerine-Arginine Splicing FactorsSRSF1 protein, humanTrans-Activatorsalternative splicingbiomarkersCP: CancerCP: Molecular biologyFLNAFOXA1HNRNPKnonsense-mediated decaypoison exonsprostate cancersplicing factorsSRSF1

Identifiers

PMID36170835
PMCPMC9532847
OpenAlexW4297373805

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.