Evidence map›Paper›PMID 29871889›Full record

ArticleThe EMBO journal2018

miR-200/375 control epithelial plasticity-associated alternative splicing by repressing the RNA-binding protein Quaking.

Katherine A Pillman, Caroline A Phillips, Suraya Roslan, John Toubia, B Kate Dredge, Andrew G Bert, Rachael Lumb, Daniel P Neumann, Xiaochun Li, Simon J Conn and 11 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 105 citations in OpenAlex.

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  14. Review
  15. Circular RNA in cancer.Nature reviews. Cancer · 2024
    Review
  16. Review
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  20. Article

8 more citing papers are in PubMed but not listed here.

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

21 authors at 3 institutions in 1 country.

Katherine A PillmanCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.ORCID 0000-0002-5869-889X
Caroline A PhillipsCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Suraya RoslanCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
John ToubiaCentre 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.
Rachael LumbCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Daniel P NeumannCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Xiaochun LiCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Simon J ConnCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.ORCID 0000-0002-1376-4515
Dawei LiuCentre 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.
David M LawrenceCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Nataly StylianouInstitute of Health and Biomedical Innovation, Australian Prostate Cancer Research Centre - Queensland, Princess Alexandra Hospital, Queensland University of Technology, Brisbane, Qld, Australia.
Andreas W SchreiberCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Wayne D TilleyDame Roma Mitchell Cancer Research Laboratories, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0003-1893-2626
Brett G HollierInstitute of Health and Biomedical Innovation, Australian Prostate Cancer Research Centre - Queensland, Princess Alexandra Hospital, Queensland University of Technology, Brisbane, Qld, Australia.
Yeesim Khew-GoodallCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.ORCID 0000-0002-0473-5392
Luke A SelthDame Roma Mitchell Cancer Research Laboratories, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0002-4686-1418
Gregory J GoodallCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia greg.goodall@unisa.edu.au philip.gregory@unisa.edu.au.ORCID 0000-0003-1294-0692
Philip A GregoryCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia greg.goodall@unisa.edu.au philip.gregory@unisa.edu.au.ORCID 0000-0002-0999-0632
South Australia Pathology · AUFreemasons Foundation Centre for Men's Health · AUQueensland University of Technology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Members of the miR-200 family are critical gatekeepers of the epithelial state, restraining expression of pro-mesenchymal genes that drive epithelial-mesenchymal transition (EMT) and contribute to metastatic cancer progression. Here, we show that miR-200c and another epithelial-enriched miRNA, miR-375, exert widespread control of alternative splicing in cancer cells by suppressing the RNA-binding protein Quaking (QKI). During EMT, QKI-5 directly binds to and regulates hundreds of alternative splicing targets and exerts pleiotropic effects, such as increasing cell migration and invasion and restraining tumour growth, without appreciably affecting mRNA levels. QKI-5 is both necessary and sufficient to direct EMT-associated alternative splicing changes, and this splicing signature is broadly conserved across many epithelial-derived cancer types. Importantly, several actin cytoskeleton-associated genes are directly targeted by both QKI and miR-200c, revealing coordinated control of alternative splicing and mRNA abundance during EMT These findings demonstrate the existence of a miR-200/miR-375/QKI axis that impacts cancer-associated epithelial cell plasticity through widespread control of alternative splicing.

Indexed as

Alternative SplicingAnimalsCell Line, TumorCell MovementCell PlasticityDogsEpithelial-Mesenchymal TransitionHumansMadin Darby Canine Kidney CellsMice, SCIDMicroRNAsRNA-Binding ProteinsMicroRNAsMIRN200 microRNA, humanMIRN375 microRNA, humanQKI protein, humanRNA-Binding Proteinsalternative splicingepithelial–mesenchymal transitionmiR‐200miR‐375Quaking

Identifiers

PMID29871889
PMCPMC6028027
OpenAlexW2807280571

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.