Evidence map›Paper›PMID 26121644›Full record

ArticlePloS one2015

Doxorubicin Activates Hepatitis B Virus Replication by Elevation of p21 (Waf1/Cip1) and C/EBPα Expression.

Yu-Fang Chen, Chin-Liew Chong, Yi-Chieh Wu, Yi-Ling Wang, Kuen-Nan Tsai, Tzer-Min Kuo, Ming-Hsiang Hong, Cheng-Po Hu, Mong-Liang Chen, Yu-Chi Chou and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

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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

11 authors at 9 institutions in 2 countries.

Yu-Fang ChenInstitute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli, Taiwan.
Chin-Liew ChongFaculty of Traditional Chinese Medicine, Southern University College, Johor Bahru, Malaysia.
Yi-Chieh WuInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli, Taiwan.
Yi-Ling WangInstitute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli, Taiwan.
Kuen-Nan TsaiInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli, Taiwan; Institute of Molecular Medicine, National Tsing Hua University, Hsinchu, Taiwan.
Tzer-Min KuoGraduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan.
Ming-Hsiang HongInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Cheng-Po HuDepartment of Life Science, Tunghai University, Taichung, Taiwan.
Mong-Liang ChenCenter for Molecular Medicine, China Medical University and Hospital, Taichung, Taiwan.
Yu-Chi ChouInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
Chungming ChangInstitute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan; Institute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli, Taiwan.
National Health Research Institutes · TWNational Yang Ming Chiao Tung University · TWChina Medical University · TWInstitute of Biomedical Sciences, Academia Sinica · TWInstitute of Molecular Biology, Academia Sinica · TWNational Tsing Hua University · TWNational Yang Ming Chiao Tung University · TWSouthern University College · MYTunghai University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus reactivation is an important medical issue in cancer patients who undergo systemic chemotherapy. Up to half of CHB carriers receiving chemotherapy develop hepatitis and among these cases a notable proportion are associated with HBV reactivation. However, the molecular mechanism(s) through which various chemotherapeutic agents induce HBV reactivation is not yet fully understood. In this study, we investigated the role of the cell cycle regulator p21 (Waf1/Cip1) in the modulation of HBV replication when a common chemotherapeutic agent, doxorubicin, is present. We showed that p21 expression was increased by doxorubicin treatment. This elevation in p21 expression enhanced the expression of CCAAT/enhancer-binding protein α (C/EBPα); such an increase is likely to promote the binding of C/EBPα to the HBV promoter, which will contribute to the activation of HBV replication. Our current study thus reveals the mechanism underlying doxorubicin modulation of HBV replication and provides an increased understanding of HBV reactivation in CHB patients who are receiving systemic chemotherapy.

Indexed as

Antibiotics, AntineoplasticCCAAT-Enhancer-Binding Protein-alphaCyclin-Dependent Kinase Inhibitor p21DoxorubicinGene ExpressionGene Expression RegulationHepatitis B virusHepatocytesHep G2 CellsHumansPromoter Regions, GeneticProtein BindingResponse ElementsRNA, ViralVirus ActivationVirus ReplicationAntibiotics, AntineoplasticCCAAT-Enhancer-Binding Protein-alphaCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DoxorubicinRNA, Viral

Identifiers

PMID26121644
PMCPMC4486450
OpenAlexW1508521111

What OpenQuestion holds

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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.