Evidence map›Paper›PMID 19578387›Full record

ArticleActa pharmacologica Sinica2009

Transformation of human liver L-O2 cells mediated by stable HBx transfection.

Wei-ying Zhang, Na Cai, Li-hong Ye, Xiao-dong Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2009. 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
1.3field-weighted citation impact, top 18% 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, 35 citations in OpenAlex.

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  10. Tripartite Motif Containing 52 (TRIM52) Promotes Cell Proliferation in Hepatitis B Virus-Associated Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  11. CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity.International journal of molecular sciences · 2017
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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

4 authors at 1 institution in 1 country.

Wei-ying ZhangDepartment of Cancer Research, Key Laboratory of Molecular Microbiology and Technology of Ministry of Education, Institute for Molecular Biology, College of Life Sciences, Nankai University, Tianjin 300071, China.
Na Cai
Li-hong Ye
Xiao-dong Zhang
Nankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo explore the mechanism of hepatocarcinogenesis associated with the hepatitis B virus X protein (HBx), we investigated the role of HBx in transformation using human liver L-O2 cells stably transfected with HBx as a model.

methodsPlasmids encoding HBx were stably transfected into immortalized human liver L-O2 cells and rodent fibroblast NIH/3T3 cells. The expression of alfa-fetoprotein (AFP), c-Myc, HBx, and survivin in the engineered cells was examined by Western blotting. The malignant phenotype of the cells was demonstrated by anchorage-independent colony formation and tumor formation in nude mice. RNA interference assays, Western blotting, luciferase reporter gene assays and flow cytometry analysis were performed. The number of centrosomes in the L-O2-X cells was determined by gamma-tubulin immunostaining. The effect of HBx on the transcriptional activity of human telomerase reverse transcriptase (hTERT) and hTERT activity in L-O2-X cells and/or 3T3-X cells was detected by the luciferase reporter gene assay and telomerase repeat amplification protocol (TRAP).

resultsStable HBx transfection resulted in a malignant phenotype in the engineered cells in vivo and in vitro. Meanwhile, HBx was able to increase the transcription of the NF-kappaB, AP-1, and survivin genes and to upregulate the expression levels of c-Myc and survivin. Abnormal centrosome duplication and activated hTERT were responsible for the transformation.

conclusionStable HBx transfection leads to genomic instability of host cells, which is responsible for hepatocarcinogenesis; meanwhile, transactivation by the HBx protein contributes to the development of hepatocellular carcinoma (HCC). The L-O2-X cell line is an ideal model for investigating the mechanism of HBx-mediated transformation.

Indexed as

Cell Transformation, NeoplasticTransfectionAnimalsCarcinoma, HepatocellularCell LineCell ProliferationCentrosomeGene Expression Regulation, NeoplasticHumansInhibitor of Apoptosis ProteinsLiverLiver NeoplasmsMiceMice, NudeMicrotubule-Associated ProteinsNF-kappa BBIRC5 protein, humanhepatitis B virus X proteinInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsNF-kappa BSurvivinTelomeraseTrans-ActivatorsTranscription Factor AP-1Viral Regulatory and Accessory Proteins

Identifiers

PMID19578387
PMCPMC4006685
OpenAlexW2089949536

What OpenQuestion holds

Textmetadata
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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.