Evidence map›Paper›PMID 28368417›Full record

ArticleOncogene2017

Oncogenic effects of evolutionarily conserved noncoding RNA ECONEXIN on gliomagenesis.

S Deguchi, K Katsushima, A Hatanaka, K Shinjo, F Ohka, T Wakabayashi, H Zong, A Natsume, Y Kondo

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  14. LncRNAInternational journal of molecular sciences · 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

9 authors at 3 institutions in 2 countries.

S DeguchiDepartment of Epigenomics, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
K KatsushimaDepartment of Epigenomics, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
A HatanakaDepartment of Epigenomics, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
K ShinjoDepartment of Epigenomics, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
F OhkaDepartment of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan.
T WakabayashiDepartment of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan.
H ZongDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA, USA.ORCID 0000-0002-4263-9633
A NatsumeDepartment of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan.
Y KondoDepartment of Epigenomics, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Nagoya City University · JPNagoya University · JPUniversity of Virginia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating studies have demonstrated the importance of long noncoding RNAs (lncRNAs) during oncogenic transformation. However, because most lncRNAs are currently uncharacterized, the identification of novel oncogenic lncRNAs is difficult. Given that intergenic lncRNA have substantially less sequence conservation patterns than protein-coding genes across species, evolutionary conserved intergenic lncRNAs are likely to be functional. The current study identified a novel intergenic lncRNA, LINC00461 (ECONEXIN) using a combined approach consisting of searching lncRNAs by evolutionary conservation and validating their expression in a glioma mouse model. ECONEXIN was the most highly conserved intergenic lncRNA containing 83.0% homology with the mouse ortholog (C130071C03Rik) for a region over 2500 bp in length within its exon 3. Expressions of ECONEXIN and C130071C03Rik were significantly upregulated in both human and mouse glioma tissues. Moreover, the expression of C130071C03Rik was upregulated even in precancerous conditions and markedly increased during glioma progression. Functional analysis of ECONEXIN in glioma cell lines, U87 and U251, showed it was dominantly located in the cytoplasm and interacted with miR-411-5p via two binding sites within ECONEXIN. Inhibition of ECONEXIN upregulated miR-411-5p together with the downregulation of its target, Topoisomerase 2 alpha (TOP2A), in glioma cell lines, resulting in decreased cell proliferation. Our data demonstrated that ECONEXIN is a potential oncogene that regulates TOP2A by sponging miR-411-5p in glioma. In addition, our investigative approaches to identify conserved lncRNA and their molecular characterization by validation in mouse tumor models may be useful to functionally annotate novel lncRNAs, especially cancer-associated lncRNAs.

Indexed as

OncogenesAnimalsAntigens, NeoplasmBrain NeoplasmsCarcinogenesisCell Line, TumorCell ProliferationConserved SequenceDisease ProgressionDNA-Binding ProteinsDNA Topoisomerases, Type IIDown-RegulationGliomaHumansMiceMicroRNAsAntigens, NeoplasmDNA-Binding ProteinsDNA Topoisomerases, Type IILINC00461 lncRNA, humanMicroRNAsMIRN411 microRNA, humanPoly-ADP-Ribose Binding ProteinsRNA-Induced Silencing ComplexRNA, Long NoncodingTOP2A protein, humanTop2a protein, mouse

Identifiers

PMID28368417
OpenAlexW2604638977

What OpenQuestion holds

Textmetadata
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.