Evidence map›Paper›PMID 37752235›Full record

ReviewOncogene2023

Epithelial specific splicing regulator proteins as emerging oncogenes in aggressive prostate cancer.

Rahul Advani, Sara Luzzi, Emma Scott, Caroline Dalgliesh, Joachim Weischenfeldt, Jennifer Munkley, David J Elliott

Open access · hybridAbstract readReview
In one paragraph

Review in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 7 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

7 authors at 2 institutions in 2 countries.

Rahul AdvaniNewcastle University Biosciences Institute (NUBI) and Newcastle University Cancer Centre, Newcastle University, Newcastle Upon Tyne, NE1 3BZ, United Kingdom.ORCID 0009-0006-9494-9584
Sara LuzziNewcastle University Biosciences Institute (NUBI) and Newcastle University Cancer Centre, Newcastle University, Newcastle Upon Tyne, NE1 3BZ, United Kingdom.ORCID 0000-0001-6337-7495
Emma ScottNewcastle University Biosciences Institute (NUBI) and Newcastle University Cancer Centre, Newcastle University, Newcastle Upon Tyne, NE1 3BZ, United Kingdom.
Caroline DalglieshNewcastle University Biosciences Institute (NUBI) and Newcastle University Cancer Centre, Newcastle University, Newcastle Upon Tyne, NE1 3BZ, United Kingdom.
Joachim WeischenfeldtBiotech Research & Innovation Centre (BRIC), The Finsen Laboratory, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0002-3917-5524
Jennifer MunkleyNewcastle University Biosciences Institute (NUBI) and Newcastle University Cancer Centre, Newcastle University, Newcastle Upon Tyne, NE1 3BZ, United Kingdom.
David J ElliottNewcastle University Biosciences Institute (NUBI) and Newcastle University Cancer Centre, Newcastle University, Newcastle Upon Tyne, NE1 3BZ, United Kingdom. David.Elliott@ncl.ac.uk.ORCID 0000-0002-6930-0699
Newcastle University · GBUniversity of Copenhagen · DK

Funding

BBSRC BB/S008039/1BBSRC BB/W002019/1Prostate Cancer UK PG12-34Prostate Cancer UK RIA16-ST2-011Prostate Cancer UK RIA21-ST2-006Prostate Cancer UK TLD-PF19-002
6 · The paper itself

Abstract

Prostate cancer progression is connected to the activity of conventional oncogenes and tumour suppressors and driven by circulating steroid hormones. A key issue has been how to identify and care for aggressively developing prostate tumours. Here we discuss how expression of the splicing regulators ESRP1 and ESRP2, and how their role as "masterminds" of epithelial splicing patterns, have been identified as markers of aggressively proliferating prostate primary tumours. We suggest that the origin of prostate cancer within epithelial cells, and the subsequent association of ESRP1 and ESRP2 expression with more aggressive disease progression, identify ESRP1 and ESRP2 as lineage survival oncogenes. To move this field on in the future it will be important to identify the gene expression targets controlled by ESRP1/2 that regulate prostate cancer proliferation. Potential future therapies could be designed to target ESRP1 and ESRP2 protein activity or their regulated splice isoforms in aggressive prostate tumours. Design of these therapies is potentially complicated by the risk of producing a more mesenchymal splicing environment that might promote tumour metastasis.

Indexed as

OncogenesProstatic NeoplasmsRNA-Binding ProteinsRNA SplicingAnimalsDisease ProgressionEpithelial CellsGene Expression Regulation, NeoplasticHumansMaleESRP1 protein, humanESRP2 protein, humanRNA-Binding Proteins

Identifiers

PMID37752235
PMCPMC10589096
OpenAlexW4387047312

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.