Evidence map›Paper›PMID 38112323›Full record

ArticleRNA biology2024

The landscape of alternative polyadenylation during EMT and its regulation by the RNA-binding protein Quaking.

Daniel P Neumann, Katherine A Pillman, B Kate Dredge, Andrew G Bert, Caroline A Phillips, Rachael Lumb, Yesha Ramani, Cameron P Bracken, Brett G Hollier, Luke A Selth and 3 more

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

Article in RNA biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

10 citing papers in PubMed, 40 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

13 authors at 6 institutions in 1 country.

Daniel P NeumannCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Katherine A PillmanCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
B Kate DredgeCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Andrew G BertCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Caroline A PhillipsCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Rachael LumbCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Yesha RamaniCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Cameron P BrackenCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Brett G HollierAustralian Prostate Cancer Research Centre - Queensland, Centre for Genomics and Personalised Health, Faculty of Health, School of Biomedical Sciences, Queensland University of Technology, Brisbane, QLD, Australia.
Luke A SelthFaculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA, Australia.
Traude H BeilharzDevelopment and Stem Cells Program, Monash Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Australia.
Gregory J GoodallCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Philip A GregoryCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
University of South Australia · AUCentre for Cancer Biology · AUSouth Australia Pathology · AUAustralian Regenerative Medicine Institute · AUFlinders University · AUQueensland University of Technology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) plays important roles in tumour progression and is orchestrated by dynamic changes in gene expression. While it is well established that post-transcriptional regulation plays a significant role in EMT, the extent of alternative polyadenylation (APA) during EMT has not yet been explored. Using 3' end anchored RNA sequencing, we mapped the alternative polyadenylation (APA) landscape following Transforming Growth Factor (TGF)-β-mediated induction of EMT in human mammary epithelial cells and found APA generally causes 3'UTR lengthening during this cell state transition. Investigation of potential mediators of APA indicated the RNA-binding protein Quaking (QKI), a splicing factor induced during EMT, regulates a subset of events including the length of its own transcript. Analysis of QKI crosslinked immunoprecipitation (CLIP)-sequencing data identified the binding of QKI within 3' untranslated regions (UTRs) was enriched near cleavage and polyadenylation sites. Following QKI knockdown, APA of many transcripts is altered to produce predominantly shorter 3'UTRs associated with reduced gene expression. These findings reveal the changes in APA that occur during EMT and identify a potential role for QKI in this process.

Indexed as

Gene Expression RegulationPolyadenylation3' Untranslated RegionsBase SequenceEpithelial-Mesenchymal TransitionHumansRNA-Binding Proteins3' Untranslated RegionsRNA-Binding Proteins3’ untranslated region (3’UTR)alternative polyadenylationCrosslinked immunopreciptation (CLIP) sequencingepithelial-mesenchymal transitionQuakingRNA binding protein (RBP)

Identifiers

PMID38112323
PMCPMC10732628
OpenAlexW4389975804

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.