Evidence map›Paper›PMID 28029658›Full record

ArticleOncotarget2017

The inhibition of 45A ncRNA expression reduces tumor formation, affecting tumor nodules compactness and metastatic potential in neuroblastoma cells.

Ilaria Penna, Arianna Gigoni, Delfina Costa, Serena Vella, Debora Russo, Alessandro Poggi, Federico Villa, Antonella Brizzolara, Claudio Canale, Andrea Mescola and 6 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 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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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

16 authors at 5 institutions in 1 country.

Ilaria PennaDepartment of Experimental Medicine (DIMES), University of Genova, Genova, Italy.
Arianna GigoniDepartment of Experimental Medicine (DIMES), University of Genova, Genova, Italy.
Delfina CostaDepartment of Experimental Medicine (DIMES), University of Genova, Genova, Italy.
Serena VellaDepartment of Laboratory Medicine and Advanced Biotechnologies, IRCCS-ISMETT (Istituto Mediterraneo per i Trapianti e Terapie ad Alta Specializzazione), Palermo, Italy.
Debora RussoIRCCS-AOU San Martino-IST, Genova, Italy.
Alessandro PoggiIRCCS-AOU San Martino-IST, Genova, Italy.
Federico VillaDepartment of Experimental Medicine (DIMES), University of Genova, Genova, Italy.
Antonella BrizzolaraDepartment of Experimental Medicine (DIMES), University of Genova, Genova, Italy.
Claudio CanaleNanophysics Unit, Italian Institute of Technology, Morego, Genova, Italy.
Andrea MescolaNanophysics Unit, Italian Institute of Technology, Morego, Genova, Italy.
Antonio DagaIRCCS-AOU San Martino-IST, Genova, Italy.
Claudio RussoDepartment of Health Sciences, University of Molise, Campobasso, Italy.
Mario NizzariDepartment of Internal Medicine (DIMI), University of Genova, Genova, Italy.
Tullio FlorioDepartment of Internal Medicine (DIMI), University of Genova, Genova, Italy.
Paola MenichiniIRCCS-AOU San Martino-IST, Genova, Italy.
Aldo PaganoDepartment of Experimental Medicine (DIMES), University of Genova, Genova, Italy.
Ospedale Policlinico San Martino · ITUniversity of Genoa · ITItalian Institute of Technology · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Molise · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We recently reported the in vitro over-expression of 45A, a RNA polymerase III-transcribed non-coding (nc)RNA, that perturbs the intracellular content of FE65L1 affecting cell proliferation rate, short-term response to genotoxic stress, substrate adhesion capacity and, ultimately, increasing the tumorigenic potential of human neuroblastoma cells. In this work, to deeply explore the mechanism by which 45A ncRNA contributes to cancer development, we targeted in vitro and in vivo 45A levels by the stable overexpression of antisense 45A RNA.45A downregulation leads to deep modifications of cytoskeleton organization, adhesion and migration of neuroblastoma cells. These effects are correlated with alterations in the expression of several genes including GTSE1 (G2 and S phase-expressed-1), a crucial regulator of tumor cell migration and metastatic potential. Interestingly, the downregulation of 45A ncRNA strongly affects the in vivo tumorigenic potential of SKNBE2 neuroblastoma cells, increasing tumor nodule compactness and reducing GTSE1 protein expression in a subcutaneous neuroblastoma mouse model. Moreover, intracardiac injection of neuroblastoma cells showed that downregulation of 45A ncRNA also influences tumor metastatic ability. In conclusion, our data highlight a key role of 45A ncRNA in cancer development and suggest that its modulation might represent a possible novel anticancer therapeutic approach.

Indexed as

Cell MovementCell ProliferationTumor BurdenAnimalsCell AdhesionCell Line, TumorDNA DamageDNA RepairDown-RegulationGene Expression Regulation, NeoplasticHEK293 CellsHumansKi-67 AntigenMice, Inbred NODMice, SCIDMicrotubule-Associated ProteinsGTSE1 protein, humanKi-67 AntigenMicrotubule-Associated ProteinsRNA, AntisenseRNA, UntranslatedSNORD45A noncoding RNA, humanGTSE1metastasisneuroblastomanon-coding RNAtumorigenesis

Identifiers

PMID28029658
PMCPMC5352393
OpenAlexW2562358288

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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.