Evidence map›Paper›PMID 29857516›Full record

ArticleInternational journal of molecular sciences2018

Mir-34a-5p Mediates Cross-Talk between M2 Muscarinic Receptors and Notch-1/EGFR Pathways in U87MG Glioblastoma Cells: Implication in Cell Proliferation.

Maria Di Bari, Valeria Bevilacqua, Antonella De Jaco, Pietro Laneve, Roberta Piovesana, Laura Trobiani, Claudio Talora, Elisa Caffarelli, Ada Maria Tata

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

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  14. miR-34a in Neurophysiology and Neuropathology.Journal of molecular neuroscience : MN · 2019
    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

9 authors at 2 institutions in 1 country.

Maria Di BariDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy. maria.dibari@uniroma1.it.
Valeria BevilacquaDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy. bevilacqua@ingm.org.
Antonella De JacoDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy. antonella.dejaco@uniroma1.it.
Pietro LaneveInstitute of Molecular Biology and Pathology, National Research Council of Italy, c/o Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy. pietro.laneve@uniroma1.it.
Roberta PiovesanaDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy. roberta.piovesana@uniroma1.it.ORCID 0000-0003-2682-4473
Laura TrobianiDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy. laura.trobiani@uniroma1.it.
Claudio TaloraDepartment of Molecular Medicine, Sapienza University of Rome, Viale Regina Elena, 291, 00161 Rome, Italy. claudio.talora@uniroma1.it.
Elisa CaffarelliInstitute of Molecular Biology and Pathology, National Research Council of Italy, c/o Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy. elisa.caffarelli@uniroma1.it.
Ada Maria TataDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy. adamaria.tata@uniroma1.it.ORCID 0000-0003-4868-5435
Sapienza University of Rome · ITInstitute of Molecular Biology and Pathology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most aggressive human brain tumor. The high growth potential and decreased susceptibility to apoptosis of the glioma cells is mainly dependent on genetic amplifications or mutations of oncogenic or pro-apoptotic genes, respectively. We have previously shown that the activation of the M2 acetylcholine muscarinic receptors inhibited cell proliferation and induced apoptosis in two GBM cell lines and cancer stem cells. The aim of this study was to delve into the molecular mechanisms underlying the M2-mediated cell proliferation arrest. Exploiting U87MG and U251MG cell lines as model systems, we evaluated the ability of M2 receptors to interfere with Notch-1 and EGFR pathways, whose activation promotes GBM proliferation. We demonstrated that the activation of M2 receptors, by agonist treatment, counteracted Notch and EGFR signaling, through different regulatory cascades depending, at least in part, on p53 status. Only in U87MG cells, which mimic p53-wild type GBMs, did M2 activation trigger a molecular circuitry involving p53, Notch-1, and the tumor suppressor mir-34a-5p. This regulatory module negatively controls Notch-1, which affects cell proliferation mainly through the Notch-1/EGFR axis. Our data highlighted, for the first time, a molecular circuitry that is deregulated in the p53 wild type GBM, based on the cross-talk between M2 receptor and the Notch-1/EGFR pathways, mediated by mir-34a-5p.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionCell Line, TumorCell ProliferationErbB ReceptorsGlioblastomaHumansMicroRNAsModels, MolecularProtein BindingReceptor, Muscarinic M2Receptor, Notch1RNA InterferenceErbB ReceptorsMicroRNAsMIRN34 microRNA, humanNOTCH1 protein, humanReceptor, Muscarinic M2Receptor, Notch1EGFRglioblastomaM2 muscarinic receptorsmir-34a-5pNotch-1p53

Identifiers

PMID29857516
PMCPMC6032387
OpenAlexW2806904698

What OpenQuestion holds

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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.