Evidence map›Paper›PMID 25427715›Full record

ArticleBMC cancer2014

Deep Sequencing the microRNA profile in rhabdomyosarcoma reveals down-regulation of miR-378 family members.

Francesca Megiorni, Samantha Cialfi, Heather P McDowell, Armando Felsani, Simona Camero, Alessandro Guffanti, Barry Pizer, Anna Clerico, Alessandra De Grazia, Antonio Pizzuti and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

47 citing papers in PubMed, 63 citations in OpenAlex.

  1. [Advances in the role of miR-378a in skeletal muscle development and diseases].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
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  7. A dysfunctional miR-1-TRPS1-MYOG axis drives ERMS by suppressing terminal myogenic differentiation.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
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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

12 authors at 3 institutions in 2 countries.

Francesca MegiorniDepartment of Paediatrics and Infantile Neuropsychiatry, Sapienza University of Rome, Viale Regina Elena 324, 00161 Rome, Italy. francesca.megiorni@uniroma1.it.
Samantha Cialfi
Heather P McDowell
Armando Felsani
Simona Camero
Alessandro Guffanti
Barry Pizer
Anna Clerico
Alessandra De Grazia
Antonio Pizzuti
Anna Moles
Carlo Dominici
Sapienza University of Rome · ITD'Appolonia (Italy) · ITAlder Hey Children's NHS Foundation Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRhabdomyosarcoma (RMS) is a highly malignant tumour accounting for nearly half of soft tissue sarcomas in children. MicroRNAs (miRNAs) represent a class of short, non-coding, regulatory RNAs which play a critical role in different cellular processes. Altered miRNA levels have been reported in human cancers, including RMS.

methodsUsing deep sequencing technology, a total of 685 miRNAs were investigated in a group of alveolar RMSs (ARMSs), embryonal RMSs (ERMSs) as well as in normal skeletal muscle (NSM). Q-PCR, MTT, cytofluorimetry, migration assay, western blot and immunofluorescence experiments were carried out to determine the role of miR-378a-3p in cancer cell growth, apoptosis, migration and differentiation. Bioinformatics pipelines were used for miRNA target prediction and clustering analysis.

resultsNinety-seven miRNAs were significantly deregulated in ARMS and ERMS when compared to NSM. MiR-378 family members were dramatically decreased in RMS tumour tissue and cell lines. Interestingly, members of the miR-378 family presented as a possible target the insulin-like growth factor receptor 1 (IGF1R), a key signalling molecule in RMS. MiR-378a-3p over-expression in an RMS-derived cell line suppressed IGF1R expression and affected phosphorylated-Akt protein levels. Ectopic expression of miR-378a-3p caused significant changes in apoptosis, cell migration, cytoskeleton organization as well as a modulation of the muscular markers MyoD1, MyoR, desmin and MyHC. In addition, DNA demethylation by 5-aza-2'-deoxycytidine (5-aza-dC) was able to up-regulate miR-378a-3p levels with a concomitant induction of apoptosis, decrease in cell viability and cell cycle arrest in G2-phase. Cells treated with 5-aza-dC clearly changed their morphology and expressed moderate levels of MyHC.

conclusionsMiR-378a-3p may function as a tumour suppressor in RMS and the restoration of its expression would be of therapeutic benefit in RMS. Furthermore, the role of epigenetic modifications in RMS deserves further investigations.

Indexed as

ApoptosisBase SequenceCell Line, TumorDNA MethylationDown-RegulationGene Expression ProfilingHigh-Throughput Nucleotide SequencingHumansMicroRNAsMolecular Sequence DataMuscle DevelopmentReceptor, IGF Type 1Receptors, SomatomedinRhabdomyosarcomaSequence AlignmentSequence Analysis, RNAIGF1R protein, humanMicroRNAsMIRN378 microRNA, humanReceptor, IGF Type 1Receptors, Somatomedin

Identifiers

PMID25427715
PMCPMC4289215
OpenAlexW2046400711

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.