Evidence map›Paper›PMID 30328580›Full record

ArticleVirologica Sinica2018

Histone Deacetylase 3 Inhibitor Suppresses Hepatitis C Virus Replication by Regulating Apo-A1 and LEAP-1 Expression.

Yuan Zhou, Qian Wang, Qi Yang, Jielin Tang, Chonghui Xu, Dongwei Gai, Xinwen Chen, Jizheng Chen

Open access · bronzeAbstract read
In one paragraph

Article in Virologica Sinica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
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  4. Review
  5. Review
  6. Article
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  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Host directed therapies: COVID-19 and beyond.Current research in pharmacology and drug discovery · 2021
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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.

Yuan ZhouState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Qian WangJiangsu Province Key Laboratory of Human Functional Genomics, Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210029, China.
Qi YangState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Jielin TangState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Chonghui XuState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Dongwei GaiState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Xinwen ChenState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Jizheng ChenState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China. chenjz@wh.iov.cn.ORCID http://orcid.org/0000-0002-2966-2388
Chinese Academy of Sciences · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase (HDAC) inhibitors show clinical promise for the treatment of cancers, including hepatocellular carcinoma (HCC). In this study, we investigated the effect of HDAC inhibitor treatment on hepatitis C virus (HCV) replication in Huh7 human liver cells and in a mouse model of HCV infection. Viral replication was markedly suppressed by the HDAC3 inhibitor at concentrations below 1 mmol/L, with no cellular toxicity. This was accompanied by upregulation of liver-expressed antimicrobial peptide 1(LEAP-1) and downregulation of apolipoprotein-A1 (Apo-A1), as determined by microarray and quantitative RT-PCR analyses. Moreover, HDAC3 was found to modulate the binding of CCAAT-enhancer-binding protein α (C/EBPα), hypoxia-inducible factor 1α (HIF1α), and signal transducer and activator of transcription 3 (STAT3) to the LEAP-1 promoter. HDAC3 inhibitor treatment also blocked HCV replication in a mouse model of HCV infection. These results indicate that epigenetic therapy with HDAC3 inhibitor may be a potential treatment for diseases associated with HCV infection such as HCC.

Indexed as

AcrylamidesAnimalsApolipoprotein A-ICarcinoma, HepatocellularCell Line, TumorHepacivirusHepcidinsHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHumansHydroxamic AcidsHypoxia-Inducible Factor 1, alpha SubunitIndolesLiver NeoplasmsMiceAcrylamidesApolipoprotein A-IHAMP protein, humanHepcidinsHIF1A protein, humanHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsHypoxia-Inducible Factor 1, alpha SubunitIndolesPCI 34051PhenylenediaminesRGFP966STAT3 protein, humanSTAT3 Transcription Factortrichostatin AApolipoprotein-A1(Apo-A1)HDAC3Hepatitis C virus (HCV)Hepatocellular carcinomaLEAP-1Viral replication

Identifiers

PMID30328580
PMCPMC6235766
OpenAlexW2896475918

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.