Evidence map›Paper›PMID 27138288›Full record

ArticleScientific reports2016

Epigenetically regulated miR-449a enhances hepatitis B virus replication by targeting cAMP-responsive element binding protein 5 and modulating hepatocytes phenotype.

Xiaoyong Zhang, Hongyan Liu, Zhanglian Xie, Wangyu Deng, Chunchen Wu, Bo Qin, Jinlin Hou, Mengji Lu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.6field-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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Cell death pathways and viruses: Role of microRNAs.Molecular therapy. Nucleic acids · 2021
    Review
  6. Review
  7. Article
  8. Article
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  11. Review
  12. Article
  13. Article
  14. Article
  15. Epigenetics and MicroRNAs in Cancer.International journal of molecular sciences · 2018
    Review
  16. miR-224 suppresses HBV replication posttranscriptionally through inhibiting SIRT1-mediated autophagy.International journal of clinical and experimental pathology · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 2 countries.

Xiaoyong ZhangInstitute of Virology, University Hospital of Essen, University of Duisburg-Essen, Essen, Germany.
Hongyan LiuState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhanglian XieState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Wangyu DengInstitute of Virology, University Hospital of Essen, University of Duisburg-Essen, Essen, Germany.
Chunchen WuInstitute of Virology, University Hospital of Essen, University of Duisburg-Essen, Essen, Germany.
Bo QinInstitute of Virology, University Hospital of Essen, University of Duisburg-Essen, Essen, Germany.
Jinlin HouState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Mengji LuInstitute of Virology, University Hospital of Essen, University of Duisburg-Essen, Essen, Germany.
University of Duisburg-Essen · DESouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular microRNAs (miRNAs) are able to influence hepatitis B virus (HBV) replication directly by binding to HBV transcripts or indirectly by targeting cellular factors. Here, we investigate the effect of epigenetically regulated miR-449a on HBV replication and the underlying mechanisms. miR-449a expression was lower in human hepatocellular carcinoma (HCC) cells than in primary hepatocytes and could be induced by trichostatin A. Ectopic miR-449a expression in HCC cells strongly enhanced HBV replication, transcription, progeny virions secretion, and antigen expression in a dose-dependent manner. miR-449a directly targeted cAMP-responsive element binding protein 5 (CREB5), which in turn induced the expression of farnesoid X receptor α (FXRα), a transcription factor that facilitates HBV replication. CREB5 knockdown and overexpression demonstrated that it is a negative regulator of HBV replication. Additionally, miR-449a overexpression inhibited proliferation, caused cell cycle arrest, and promoted HCC cell differentiation. The results indicated that epigenetically regulated miR-449a targets CREB5 to increase FXRα expression, thereby promoting HBV replication and gene expression. Our findings provide a new understanding of the role of miRNAs in HBV replication.

Indexed as

Carcinoma, HepatocellularCell DifferentiationCell Line, TumorCyclic AMP Response Element-Binding Protein AEpigenesis, GeneticGene Expression Regulation, NeoplasticHepatitis BHepatitis B virusHepatocytesHumansLiver NeoplasmsMicroRNAsReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearVirus ReplicationCREB5 protein, humanCyclic AMP Response Element-Binding Protein AMicroRNAsMIRN449 microRNA, humanReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and Nuclear

Identifiers

PMID27138288
PMCPMC4853741
OpenAlexW2345430579

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.