ArticlePloS one2013
Liver-specific expressions of HBx and src in the p53 mutant trigger hepatocarcinogenesis in zebrafish.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
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- Phenotypic Response Surfaces-Guided Optimization (PRS-OPT) of Propolis-Metformin-Regorafenib Combination Therapy for MASLD-Associated Hepatocellular Carcinoma.Oncology research · 2026Article
- New Progress in Zebrafish Liver Tumor Models: Techniques and Applications in Hepatocellular Carcinoma Research.International journal of molecular sciences · 2025Review
- Creatine and L-carnitine attenuate muscular laminopathy in the LMNA mutation transgenic zebrafish.Scientific reports · 2024Article
- The oncogenic role of hepatitis B virus X gene in hepatocarcinogenesis: recent updates.Exploration of targeted anti-tumor therapy · 2024Review
- Methods to Study Liver Disease Using Zebrafish Larvae.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Advantages of the zebrafish tumor xenograft model: the evaluation of efficacy in cancer therapy and the application to the study of lncRNAs.Frontiers in immunology · 2024Review
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- Effect of Lipopolysaccharides on Liver Tumor Metastasis ofBiomedicines · 2022Article
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- L-Carnitine ameliorates congenital myopathy in a tropomyosin 3 de novo mutation transgenic zebrafish.Journal of biomedical science · 2021Article
- Low molecular weight fucoidan inhibits hepatocarcinogenesis and nonalcoholic fatty liver disease in zebrafish via ASGR/STAT3/HNF4A signaling.Clinical and translational medicine · 2020Article
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- Genetic Engineering of Zebrafish in Cancer Research.Cancers · 2020Review
- Low Molecular Weight Fucoidan Prevents Radiation-Induced Fibrosis and Secondary Tumors in a Zebrafish Model.Cancers · 2020Article
- Transcriptomically Revealed Oligo-Fucoidan Enhances the Immune System and Protects Hepatocytes via the ASGPR/STAT3/HNF4A Axis.Biomolecules · 2020Article
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- Modeling of Solid-Tumor Microenvironment in Zebrafish (Danio Rerio) Larvae.Advances in experimental medicine and biology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocarcinogenesis is a multistep process that starts from fatty liver and transitions to fibrosis and, finally, into cancer. Many etiological factors, including hepatitis B virus X antigen (HBx) and p53 mutations, have been implicated in hepatocarcinogenesis. However, potential synergistic effects between these two factors and the underlying mechanisms by which they promote hepatocarcinogenesis are still unclear. In this report, we show that the synergistic action of HBx and p53 mutation triggers progressive hepatocellular carcinoma (HCC) formation via src activation in zebrafish. Liver-specific expression of HBx in wild-type zebrafish caused steatosis, fibrosis and glycogen accumulation. However, the induction of tumorigenesis by HBx was only observed in p53 mutant fish and occurred in association with the up-regulation and activation of the src tyrosine kinase pathway. Furthermore, the overexpression of src in p53 mutant zebrafish also caused hyperplasia, HCC, and sarcomatoid HCC, which were accompanied by increased levels of the signaling proteins p-erk, p-akt, myc, jnk1 and vegf. Increased expression levels of lipogenic factors and the genes involved in lipid metabolism and glycogen storage were detected during the early stages of hepatocarcinogenesis in the HBx and src transgenic zebrafish. The up-regulation of genes involved in cell cycle regulation, tumor progression and other molecular hallmarks of human liver cancer were found at later stages in both HBx and src transgenic, p53 mutant zebrafish. Together, our study demonstrates that HBx and src overexpression induced hepatocarcinogenesis in p53 mutant zebrafish. This phenomenon mimics human HCC formation and provides potential in vivo platforms for drug screening for therapies for human liver cancer.
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