Evidence map›Paper›PMID 38779518›Full record

ArticleJournal of clinical and translational hepatology2024

Paclitaxel-induced Immune Dysfunction and Activation of Transcription Factor AP-1 Facilitate Hepatitis B Virus Replication.

Shi Chen, Benhua Li, Wei Luo, Adeel Ur Rehman, Miao He, Qian Yang, Shunyao Wang, Jinjun Guo, Ling Chen, Xiaosong Li

Abstract read
In one paragraph

Article in Journal of clinical and translational hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Review
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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

10 authors.

Shi ChenClinical Molecular Medicine Testing Center, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Benhua LiClinical Molecular Medicine Testing Center, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Wei LuoAffiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Adeel Ur RehmanClinical Molecular Medicine Testing Center, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Miao HeLaboratory Animal Center of Chongqing Medical University, Chongqing, China.
Qian YangClinical Molecular Medicine Testing Center, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Shunyao WangClinical Molecular Medicine Testing Center, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Jinjun GuoBishan Hospital of Chongqing, Bishan Hospital of Chongqing Medical University, Chongqing, China.
Ling ChenThe Center of Experimental Teaching Management, Chongqing Medical University, Chongqing, China.ORCID https://orcid.org/0000-0003-4391-2432
Xiaosong LiClinical Molecular Medicine Testing Center, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China.ORCID https://orcid.org/0000-0001-5533-7995

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Aims: Hepatitis B virus (HBV) reactivation is commonly observed in individuals with chronic HBV infection undergoing antineoplastic drug therapy. Paclitaxel (PTX) treatment has been identified as a potential trigger for HBV reactivation. This study aimed to uncover the mechanisms of PTX-induced HBV reactivation Methods: The impact of PTX on HBV replication was assessed through various methods including enzyme-linked immunosorbent assay, dual-luciferase reporter assay, quantitative real-time PCR, chromatin immunoprecipitation, and immunohistochemical staining. Transcriptome sequencing and 16S rRNA sequencing were employed to assess alterations in the transcriptome and microbial diversity in PTX-treated HBV transgenic mice. Results: PTX enhanced the levels of HBV 3.5-kb mRNA, HBV DNA, HBeAg, and HBsAg both Conclusions: PTX-induced HBV reactivation was likely a synergistic outcome of immune suppression and direct stimulation of HBV replication through the enhancement of HBV core promoter activity mediated by the transcription factor AP-1. These findings propose a novel molecular mechanism, underscoring the critical role of AP-1 in PTX-induced HBV reactivation.

Indexed as

AP-1Gut microbiotaHBV reactivationImmune systemPaclitaxelTranscription factor

Identifiers

PMID38779518
PMCPMC11106347

What OpenQuestion holds

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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.