Evidence map›Paper›PMID 24401568›Full record

ArticleAutophagy2014

Hepatitis B virus X protein inhibits autophagic degradation by impairing lysosomal maturation.

Bo Liu, Mengdie Fang, Ye Hu, Baoshan Huang, Ning Li, Chunmei Chang, Rui Huang, Xiao Xu, Zhenggang Yang, Zhi Chen and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

113 citing papers in PubMed, 1 synthesis or guideline pooled it, 190 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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53 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Bo LiuDepartment of Biochemistry and Molecular Biology; Program in Molecular Cell Biology; Zhejiang University School of Medicine; Hangzhou, Zhejiang, China.
Mengdie FangDepartment of Biochemistry and Molecular Biology; Program in Molecular Cell Biology; Zhejiang University School of Medicine; Hangzhou, Zhejiang, China.
Ye HuDepartment of Biochemistry and Molecular Biology; Program in Molecular Cell Biology; Zhejiang University School of Medicine; Hangzhou, Zhejiang, China.
Baoshan HuangDepartment of Biochemistry and Molecular Biology; Program in Molecular Cell Biology; Zhejiang University School of Medicine; Hangzhou, Zhejiang, China.
Ning LiDepartment of Biochemistry and Molecular Biology; Program in Molecular Cell Biology; Zhejiang University School of Medicine; Hangzhou, Zhejiang, China.
Chunmei ChangDepartment of Biochemistry and Molecular Biology; Program in Molecular Cell Biology; Zhejiang University School of Medicine; Hangzhou, Zhejiang, China.
Rui HuangDepartment of Biochemistry and Molecular Biology; Program in Molecular Cell Biology; Zhejiang University School of Medicine; Hangzhou, Zhejiang, China.
Xiao XuDepartment of Surgery; First Affiliated Hospital; Zhejiang University School of Medicine; Hangzhou, Zhejiang China.
Zhenggang YangState Key Laboratory for Diagnosis and Treatment of Infectious Diseases; First Affiliated Hospital; Zhejiang University School of Medicine; Hangzhou, Zhejiang China.
Zhi ChenState Key Laboratory for Diagnosis and Treatment of Infectious Diseases; First Affiliated Hospital; Zhejiang University School of Medicine; Hangzhou, Zhejiang China.
Wei LiuDepartment of Biochemistry and Molecular Biology; Program in Molecular Cell Biology; Zhejiang University School of Medicine; Hangzhou, Zhejiang, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, First Affiliated Hospital; Zhejiang University School of Medicine; Hangzhou, Zhejiang China.
Zhejiang University · CNInstitute of Molecular and Cell Biology · RUState Key Laboratory of Diagnosis and Treatment of Infectious Diseases

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deficiency in autophagy, a lysosome-dependent cell degradation pathway, has been associated with a variety of diseases especially cancer. Recently, the activation of autophagy by hepatitis B virus X (HBx) protein, which is implicated in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC), has been identified in hepatic cells. However, the underlying mechanism and the relevance of HBx-activated autophagy to the carcinogenesis caused by HBV remain elusive. Here, by transfection of HBV genomic DNA and HBx in hepatic and hepatoma cells, we showed that HBV- or HBx-induced autophagosome formation was accompanied by unchanged MTOR (mechanistic target of rapamycin) activity and decreased degradation of LC3 and SQSTM1/p62, the typical autophagic cargo proteins. Further functional and morphological analysis indicated that HBx dramatically impaired lysosomal acidification leading to a drop in lysosomal degradative capacity and the accumulation of immature lysosomes possibly through interaction with V-ATPase affecting its lysosome targeting. Moreover, clinical specimen test showed increased SQSTM1 and immature lysosomal hydrolase CTSD (cathepsin D) in human liver tissues with chronic HBV infection and HBV-associated liver cancer. These data suggest that a repressive effect of HBx on lysosomal function is responsible for the inhibition of autophagic degradation, and this may be critical to the development of HBV-associated HCC.

Indexed as

AutophagyCarcinoma, HepatocellularCell Line, TumorHepatitis B virusHepatocytesHumansLiver NeoplasmsLysosomesTrans-ActivatorsViral Regulatory and Accessory Proteinshepatitis B virus X proteinTrans-ActivatorsViral Regulatory and Accessory Proteinsautophagyhepatitis B virushepatitis B virus X proteinhepatocellular carcinomalysosome

Identifiers

PMID24401568
PMCPMC4077881
OpenAlexW2003858076

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.