Evidence map›Paper›PMID 24627491›Full record

ArticleThe Journal of biological chemistry2014

Specificity protein 1 (Sp1) maintains basal epithelial expression of the miR-200 family: implications for epithelial-mesenchymal transition.

Natasha Kolesnikoff, Joanne L Attema, Suraya Roslan, Andrew G Bert, Quenten P Schwarz, Philip A Gregory, Gregory J Goodall

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
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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 3 institutions in 1 country.

Natasha KolesnikoffCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Joanne L AttemaCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia,; Discipline of Medicine, The University of Adelaide, Adelaide, South Australia 5005, Australia, and.
Suraya RoslanCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Andrew G BertCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Quenten P SchwarzCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Philip A GregoryCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia,; Discipline of Medicine, The University of Adelaide, Adelaide, South Australia 5005, Australia, and. Electronic address: philip.gregory@health.sa.gov.au.
Gregory J GoodallCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia,; Discipline of Medicine, The University of Adelaide, Adelaide, South Australia 5005, Australia, and; School of Molecular and Biomedical Science, The University of Adelaide, Adelaide, South Australia 5005, Australia. Electronic address: greg.goodall@health.sa.gov.au.
South Australia Pathology · AUUniversity of Adelaide · AUUniversity of South Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is required for the specification of tissues during embryonic development and is recapitulated during the metastatic progression of tumors. The miR-200 family plays a critical role in enforcing the epithelial state with their expression lost in cells undergoing EMT. EMT can be mediated by activation of the ZEB1 and ZEB2 (ZEB) transcription factors, which repress miR-200 expression via a self-reinforcing double negative feedback loop to promote the mesenchymal state. However, it remains unclear what factors drive and maintain epithelial-specific expression of miR-200 in the absence of EMT-inducing factors. Here, we show that the transcription factor Specificity Protein 1 (Sp1) binds to the miR-200b∼200a∼429 proximal promoter and activates miR-200 expression in epithelial cells. In mesenchymal cells, Sp1 expression is maintained, but its ability to activate the miR-200 promoter is perturbed by ZEB-mediated repression. Reduction of Sp1 expression caused changes in EMT-associated markers in epithelial cells. Furthermore, we observed co-expression of Sp1 and miR-200 during mouse embryonic development wherein miR-200 expression was only lost in regions with high ZEB expression. Together, these findings indicate that miR-200 family members require Sp1 to drive basal expression and to maintain an epithelial state.

Indexed as

AnimalsCell Line, TumorDogsEmbryo, MammalianEmbryonic DevelopmentEpithelial-Mesenchymal TransitionGene Expression Regulation, DevelopmentalHomeodomain ProteinsHumansKruppel-Like Transcription FactorsMadin Darby Canine Kidney CellsMiceMicroRNAsRepressor ProteinsResponse ElementsSp1 Transcription FactorHomeodomain ProteinsKruppel-Like Transcription FactorsMicroRNAsMIRN200 microRNA, humanMirn200 microRNA, mouseRepressor ProteinsSp1 Transcription FactorTranscription FactorsZEB1 protein, humanZEB1 protein, mouseZEB2 protein, humanZEB2 protein, mouseZinc Finger E-box-Binding Homeobox 1Zinc Finger E-box Binding Homeobox 2Epithelial mesenchymal transitionMetastasisMicroRNAmiR-200Sp1TranscriptionZEB transcription factor

Identifiers

PMID24627491
PMCPMC4036258
OpenAlexW2079077785

What Socratic holds

Textmetadata
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 Socratic graph.