Evidence map›Paper›PMID 26203557›Full record

ArticleOncotarget2015

miR-200c dampens cancer cell migration via regulation of protein kinase A subunits.

Florian Christoph Sigloch, Ulrike Christina Burk, Martin Lothar Biniossek, Thomas Brabletz, Oliver Schilling

Abstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
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  7. Effect of Stromal Cells in Tumor Microenvironment on Metastasis Initiation.International journal of biological sciences · 2018
    Review
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  15. Regulation of epithelial-mesenchymal transition through microRNAs: clinical and biological significance of microRNAs in breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  16. miR-200c: a versatile watchdog in cancer progression, EMT, and drug resistance.Journal of molecular medicine (Berlin, Germany) · 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

5 authors.

Florian Christoph SiglochInstitute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, Freiburg, Germany.
Ulrike Christina BurkInstitute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, Freiburg, Germany.
Martin Lothar BiniossekInstitute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, Freiburg, Germany.
Thomas BrabletzExperimental Medicine I, Nikolaus-Fiebiger-Center for Molecular Medicine, University Erlangen-Nürnberg, Erlangen, Germany.
Oliver SchillingInstitute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expression of miR-200c is a molecular switch to determine cellular fate towards a mesenchymal or epithelial phenotype. miR-200c suppresses the early steps of tumor progression by preventing epithelial-mesenchymal transition (EMT) and intravasation of tumor cells. Unraveling the underlying molecular mechanisms might pinpoint to novel therapeutic options. To better understand these mechanisms it is crucial to identify targets of miR-200c. Here, we employ a combination of quantitative proteomic and bioinformatic strategies to identify novel miR-200c targets. We identify and confirm two subunits of the central cellular kinase protein kinase A (PKA), namely PRKAR1A and PRKACB, to be directly regulated by miR-200c. Notably, siRNA-mediated downregulation of both proteins phenocopies the migratory behavior of breast cancer cells after miR-200c overexpression. Patient data from publicly accessible databases supports a miR-200c-PKA axis. Thus, our study identifies the PKA heteroprotein as an important mediator of miR-200c induced repression of migration in breast cancer cells. By bioinformatics, we define a miRNA target cluster consisting of PRKAR1A, PRKAR2B, PRKACB, and COF2, which is targeted by a group of 14 miRNAs.

Indexed as

Breast NeoplasmsCell Line, TumorCell MovementChromatography, LiquidCyclic AMP-Dependent Protein Kinase Catalytic SubunitsCyclic AMP-Dependent Protein Kinase RIalpha SubunitEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansLim KinasesMicroRNAsRNA InterferenceRNA, Small InterferingTandem Mass SpectrometryCyclic AMP-Dependent Protein Kinase Catalytic SubunitsCyclic AMP-Dependent Protein Kinase RIalpha SubunitLIMK1 protein, humanLim KinasesMicroRNAsMIRN200 microRNA, humanPRKACB protein, humanPRKAR1A protein, humanRNA, Small InterferingcofilinmiR-200cmiRNA target clusterPKAproteomics

Identifiers

PMID26203557
PMCPMC4695158

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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.