Evidence map›Paper›PMID 33543022›Full record

ArticleMatrix biology plus2020

miR-200b restrains EMT and aggressiveness and regulates matrix composition depending on ER status and signaling in mammary cancer.

Zoi Piperigkou, Marco Franchi, Christoph Riethmüller, Martin Götte, Nikos K Karamanos

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Matrix biology plus, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

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  13. Frontiers in oncology · 2022
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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

5 authors at 4 institutions in 3 countries.

Zoi PiperigkouBiochemistry, Biochemical Analysis & Matrix Pathobiology Research Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras, Patras, Greece.
Marco FranchiDepartment for Life Quality Studies, University of Bologna, Rimini, Italy.
Christoph RiethmüllerCentre for Nanotechnology, Serend-ip GmbH, Münster, Germany.
Martin GötteDepartment of Gynecology and Obstetrics, Münster University Hospital, Münster, Germany.
Nikos K KaramanosBiochemistry, Biochemical Analysis & Matrix Pathobiology Research Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras, Patras, Greece.
University of Patras · GRCeNTech · DEUniversity Hospital Münster · DEUniversity of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Secreted microRNAs (miRNAs) reside in a complex regulatory network with extracellular matrix (ECM) macromolecules, which affect cell-cell communication, therefore miRNA expression highlights its significance in several aspects of human diseases, including cancer. miRNA-mediated regulation of breast cancer has received considerable attention due to evidence that shows miRNAs to mediate estrogen receptor (ER) status, metastasis, chemoresistance and epithelial-to-mesenchymal transition (EMT). miR-200b is a pluripotent miRNA, which is inversely regulated by ERα and ERβ in mammary cancer. It has been identified as tumor suppressor and EMT inhibitor serving as a critical biomarker, as its expression in breast tumor determines the disease-free survival, thus highlighting its roles in breast cancer invasion and metastasis. The main goal of this study was to investigate the role of miR-200b in modulating the behavior of breast cancer cells with different ER status. We demonstrate that estrogen signaling through ERs reduces miR-200b expression levels in ERα-positive breast cancer cells. Moreover, miR-200b upregulation reduces the aggressive phenotype of ERβ-positive breast cancer cells by inhibiting cell invasiveness and motility, followed by ECM reorganization as well as cytoskeletal and morphological changes concluded from deep inspection of cell topography. Future investigation towards the mechanistic perspective of miR-200b effects in the behavior of aggressive mammary cancer cells appears rewarding in order to expand our understanding of miR-200b as a novel mediator beyond breast cancer diagnosis and pharmaceutical targeting.

Indexed as

Breast cancerECM, extracellular matrixEGFR, epidermal growth factor receptorEMT, epithelial-to-mesenchymal-transitionER, estrogen receptorErk, extracellular signal-regulated kinaseEstrogen receptorsExtracellular matrixGAG, glycosaminoglycanGF, growth factorHER2, human epidermal growth factor receptor 2IGF-IR, insulin-like growth factor receptor type IIL, interleukinmiR-200bmiRNA, microRNAmiRNAsMMP, matrix metalloproteinasePG, proteoglycanpre-miRNA, precursor miRNAPR, progesterone receptorRISC, RNA-induced silencing complexSERM, selective estrogen receptor modulatorTGFβ, transforming growth factor beta

Identifiers

PMID33543022
PMCPMC7852204
OpenAlexW3000858733

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Registered trials

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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.