Evidence map›Paper›PMID 29073265›Full record

ArticlePloS one2017

MiRNA-124 is a link between measles virus persistent infection and cell division of human neuroblastoma cells.

Hila Naaman, Glenn Rall, Christine Matullo, Isana Veksler-Lublinsky, Yonat Shemer-Avni, Jacob Gopas

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. miRNA Target Prediction: An Overview of the Past and Current Tools.Methods in molecular biology (Clifton, N.J.) · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
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

6 authors at 2 institutions in 2 countries.

Hila NaamanThe Shraga Segal Department of Microbiology and Immunology and Genetics, Faculty of Health Sciences Ben-Gurion University of the Negev, Beer Sheva, Israel.
Glenn RallFox Chase Cancer Center, Blood Cell Development and Function, Philadelphia, Pennsylvania, United States of America.
Christine MatulloFox Chase Cancer Center, Blood Cell Development and Function, Philadelphia, Pennsylvania, United States of America.
Isana Veksler-LublinskySoftware and Information Systems Engineering, Ben-Gurion University of the Negev, Beer Sheva, Israel.
Yonat Shemer-AvniThe Shraga Segal Department of Microbiology and Immunology and Genetics, Faculty of Health Sciences Ben-Gurion University of the Negev, Beer Sheva, Israel.
Jacob GopasThe Shraga Segal Department of Microbiology and Immunology and Genetics, Faculty of Health Sciences Ben-Gurion University of the Negev, Beer Sheva, Israel.ORCID http://orcid.org/0000-0001-9289-8898
Ben-Gurion University of the Negev · ILFox Chase Cancer Center · US

Funding

The Role of Host-Encoded microRNAs in Maintaining Measles Virus PersistenceR03AI094164 · NIAID · RESEARCH INST OF FOX CHASE CAN CTR · PI RALL, GLENN F · 2012 to 2013
$143k
NIAID NIH HHS R03 AI094164
6 · The paper itself

Abstract

Measles virus (MV) infects a variety of lymphoid and non-lymphoid peripheral organs. However, in rare cases, the virus can persistently infect cells within the central nervous system. Although some of the factors that allow MV to persist are known, the contribution of host cell-encoded microRNAs (miRNA) have not been described. MiRNAs are a class of noncoding RNAs transcribed from genomes of all multicellular organisms and some viruses, which regulate gene expression in a sequence-specific manner. We have studied the contribution of host cell-encoded miRNAs to the establishment of MV persistent infection in human neuroblastoma cells. Persistent MV infection was accompanied by differences in the expression profile and levels of several host cell-encoded microRNAs as compared to uninfected cells. MV persistence infection of a human neuroblastoma cell line (UKF-NB-MV), exhibit high miRNA-124 expression, and reduced expression of cyclin dependent kinase 6 (CDK6), a known target of miRNA-124, resulting in slower cell division but not cell death. By contrast, acute MV infection of UKF-NB cells did not result in increased miRNA-124 levels or CDK6 reduction. Ectopic overexpression of miRNA-124 affected cell viability only in UKF-NB-MV cells, causing cell death; implying that miRNA-124 over expression can sensitize cells to death only in the presence of MV persistent infection. To determine if miRNA-124 directly contributes to the establishment of MV persistence, UKF-NB cells overexpressing miRNA-124 were acutely infected, resulting in establishment of persistently infected colonies. We propose that miRNA-124 triggers a CDK6-dependent decrease in cell proliferation, which facilitates the establishment of MV persistence in neuroblastoma cells. To our knowledge, this is the first report to describe the role of a specific miRNA in MV persistence.

Indexed as

ApoptosisCell DivisionCell Line, TumorCyclin-Dependent Kinase 6Down-RegulationHumansMeaslesMicroRNAsNeuroblastomaCyclin-Dependent Kinase 6MicroRNAsMIRN124 microRNA, human

Identifiers

PMID29073265
PMCPMC5658143
OpenAlexW2766486366

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.