Evidence map›Paper›PMID 30042818›Full record

ArticleOncotarget2018

Screening of microRNAs for a repressor of hepatitis B virus replication.

Yutaka Naito, Susumu Hamada-Tsutsumi, Yusuke Yamamoto, Akiko Kogure, Yusuke Yoshioka, Koichi Watashi, Takahiro Ochiya, Yasuhito Tanaka

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Article
  5. Article
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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

8 authors at 2 institutions in 1 country.

Yutaka Naito *Division of Molecular and Cellular Medicine, National Cancer Center Research Institute, Tokyo, Japan.
Susumu Hamada-Tsutsumi *Department of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Yusuke YamamotoDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, Tokyo, Japan.
Akiko KogureDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, Tokyo, Japan.
Yusuke YoshiokaDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, Tokyo, Japan.
Koichi WatashiDepartment of Virology II, National Institute of Infectious Diseases, Tokyo, Japan.
Takahiro OchiyaDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, Tokyo, Japan.
Yasuhito TanakaDepartment of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Nagoya City University · JPNational Institute of Infectious Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatitis B virus (HBV) infection is a leading cause of persistent liver diseases, cirrhosis and hepatocellular carcinoma (HCC) worldwide. Since deregulation of microRNA (miRNA) expression by HBV infection contributes to enhanced viral replication and pathogenesis, modulation of miRNA activity can be a novel therapeutic approach towards HBV eradication. As the effects of the vast majority of miRNAs on HBV replication have not been empirically investigated, here, we aim to identify novel therapeutic targets that have a strong antiviral effect on HBV.

methodsHepG2-hNTCP-C4 cells were infected with HBV, and then were individually transfected with the library mimics of 2048 miRNAs. To assess the amount of intracellular and extracellular DNA and HBsAg, qPCR and ELISA were performed respectively.

resultsFrom miRNA library screening, we identified 39 miRNAs as candidate repressors of HBV replication. Among them, 9 miRNAs, including miR-204, strongly decreased both HBV DNA and HBsAg in culture supernatant of HepG2-hNTCP-C4 cells. Furthermore, we also showed that inhibition of Rab22a, one of the targets of miR-204, also suppressed intracellular and extracellular HBV DNA expression in HepG2.2.15.7 cells.

conclusionsOur findings contribute to the understanding of the roles of miRNAs underlying HBV replication and show the possibility of developing a novel strategy for miRNA-mediated HBV treatment.

Indexed as

hepatitis B virusmicroRNAmiR-204Rab22a

Identifiers

PMID30042818
PMCPMC6057454
OpenAlexW2821850927

What OpenQuestion holds

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LicenceCC BY
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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.