Evidence map›Paper›PMID 22384255›Full record

ArticlePloS one2012

Cooperation of p300 and PCAF in the control of microRNA 200c/141 transcription and epithelial characteristics.

Yoshiaki Mizuguchi, Susan Specht, John G Lunz, Kumiko Isse, Natasha Corbitt, Toshihiro Takizawa, Anthony J Demetris

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 56 citations in OpenAlex.

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  9. Acquired temozolomide resistance in MGMTCell death & disease · 2022
    Article
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  20. Epigenetic regulation of epithelial-mesenchymal transition.Cellular and molecular life sciences : CMLS · 2016
    Review
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.

Yoshiaki MizuguchiThomas E Starzl Transplantation Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.
Susan Specht
John G Lunz
Kumiko Isse
Natasha Corbitt
Toshihiro Takizawa
Anthony J Demetris
University of Pittsburgh Medical Center · USNippon Medical School · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial to mesenchymal transition (EMT) not only occurs during embryonic development and in response to injury, but is an important element in cancer progression. EMT and its reverse process, mesenchymal to epithelial transition (MET) is controlled by a network of transcriptional regulators and can be influenced by posttranscriptional and posttranslational modifications. EMT/MET involves many effectors that can activate and repress these transitions, often yielding a spectrum of cell phenotypes. Recent studies have shown that the miR-200 family and the transcriptional suppressor ZEB1 are important contributors to EMT. Our previous data showed that forced expression of SPRR2a was a powerful inducer of EMT and supports the findings by others that SPRR gene members are highly upregulated during epithelial remodeling in a variety of organs. Here, using SPRR2a cells, we characterize the role of acetyltransferases on the microRNA-200c/141 promoter and their effect on the epithelial/mesenchymal status of the cells. We show that the deacetylase inhibitor TSA as well as P300 and PCAF can cause a shift towards epithelial characteristics in HUCCT-1-SPRR2a cells. We demonstrate that both P300 and PCAF act as cofactors for ZEB1, forming a P300/PCAF/ZEB1 complex on the miR200c/141 promoter. This binding results in lysine acetylation of ZEB1 and a release of ZEB1 suppression on miR-200c/141 transcription. Furthermore, disruption of P300 and PCAF interactions dramatically down regulates miR-200c/141 promoter activity, indicating a PCAF/P300 cooperative function in regulating the transcriptional suppressor/activator role of ZEB1. These data demonstrate a novel mechanism of miRNA regulation in mediating cell phenotype.

Indexed as

AnimalsCell Line, TumorCornified Envelope Proline-Rich ProteinsEpithelial-Mesenchymal TransitionEpitheliumHumansMiceMicroRNAsModels, Geneticp300-CBP-Associated Factorp300-CBP Transcription FactorsPhenotypePromoter Regions, GeneticProtein BiosynthesisTranscription, GeneticUp-RegulationCornified Envelope Proline-Rich ProteinsMicroRNAsMIRN141 microRNA, humanMirn141 microRNA, mouseMIRN200 microRNA, humanMirn200 microRNA, mousep300-CBP-Associated Factorp300-CBP Transcription FactorsSprr2a1 protein, mouseSPRR2A protein, human

Identifiers

PMID22384255
PMCPMC3284570
OpenAlexW2033660315

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.