Evidence map›Paper›PMID 28159925›Full record

ArticleOncotarget2017

miRNA-1246 induces pro-inflammatory responses in mesenchymal stem/stromal cells by regulating PKA and PP2A.

Alexander Bott, Nese Erdem, Shalom Lerrer, Agnes Hotz-Wagenblatt, Christian Breunig, Khalid Abnaof, Angelika Wörner, Heike Wilhelm, Ewald Münstermann, Adit Ben-Baruch and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.6field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

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  20. Deciphering the role of microRNAs in mustard gas-induced toxicity.Annals of the New York Academy of Sciences · 2021
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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

11 authors at 3 institutions in 2 countries.

Alexander BottDivision of Molecular Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Nese ErdemDivision of Molecular Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Shalom LerrerDepartment of Cell Research and Immunology, Tel Aviv University, Tel Aviv, Israel.
Agnes Hotz-WagenblattBioinformatics Group, Genomics & Proteomics Core Facility (GPCF), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Christian BreunigDivision of Molecular Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Khalid AbnaofDivision of Molecular Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Angelika WörnerDivision of Molecular Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Heike WilhelmDivision of Molecular Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Ewald MünstermannDivision of Molecular Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Adit Ben-BaruchDepartment of Cell Research and Immunology, Tel Aviv University, Tel Aviv, Israel.
Stefan WiemannDivision of Molecular Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
German Cancer Research Center · DEHeidelberg University · DETel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor microenvironment (TME) has an impact on breast cancer progression by creating a pro-inflammatory milieu within the tumor. However, little is known about the roles of miRNAs in cells of the TME during this process. We identified six putative oncomiRs in a breast cancer dataset, all strongly correlating with poor overall patient survival. Out of the six candidates, miR-1246 was upregulated in aggressive breast cancer subtypes and expressed at highest levels in mesenchymal stem/stroma cells (MSCs). Functionally, miR-1246 led to a p65-dependent increase in transcription and release of pro-inflammatory mediators IL-6, CCL2 and CCL5 in MSCs, and increased NF-κB activity. The pro-inflammatory phenotype of miR-1246 in MSCs was independent of TNFα stimulations and mediated by direct targeting of the tumor-suppressors PRKAR1A and PPP2CB. In vitro recapitulation of the TME revealed increased Stat3 phosphorylation in breast epithelial (MCF10A) and cancer cells (SK-BR-3, MCF7, T47D) upon incubation with conditioned medium (CM) of MSCs overexpressing miR-1246. Additionally, this stimulation enhanced proliferation of MCF10A cells, increased migration of MDA-MB-231 cells and induced attraction of THP-1 monocytic cells. Our data shows that miR-1246 acts as both key-enhancer of pro-inflammatory responses in MSCs and putative oncomiR in breast cancer, suggesting its influence on cancer-related inflammation and breast cancer progression.

Indexed as

Gene Expression Regulation3' Untranslated RegionsBreast NeoplasmsCell Line, TumorCyclic AMP-Dependent Protein Kinase RIalpha SubunitCyclic AMP-Dependent Protein KinasesFemaleGene Knockdown TechniquesHumansInflammationMesenchymal Stem CellsMicroRNAsNF-kappa BProtein Phosphatase 2RNA InterferenceSignal Transduction3' Untranslated RegionsCyclic AMP-Dependent Protein Kinase RIalpha SubunitCyclic AMP-Dependent Protein KinasesMicroRNAsMIRN1246 microRNA, humanNF-kappa BPPP2CB protein, humanPRKAR1A protein, humanProtein Phosphatase 2Tumor Necrosis Factor-alphabreast cancermesenchymal stem/stromal cellmicroRNANF-kappaB signalingtumor microenvironment

Identifiers

PMID28159925
PMCPMC5546423
OpenAlexW2585803500

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.