ArticleScientific reports2016
Development of a conditional liver tumor model by mifepristone-inducible Cre recombination to control oncogenic kras V12 expression in transgenic zebrafish.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 15 citations in OpenAlex.
- Cancer Modeling by Transgene Electroporation in Adult Zebrafish (TEAZ).Methods in molecular biology (Clifton, N.J.) · 2024Article
- Zebrafish-based platform for emerging bio-contaminants and virus inactivation research.The Science of the total environment · 2023Review
- Zebrafish as an experimental model for the simulation of neurological and craniofacial disorders.Veterinary world · 2022Review
- Review
- Genetic Engineering of Zebrafish in Cancer Research.Cancers · 2020Review
- Transgenic strategies to generate heterogeneous hepatic cancer models in zebrafish.Journal of molecular cell biology · 2019Article
- Inducible Intestine-Specific Expression of krasNeoplasia (New York, N.Y.) · 2018Article
- Development of a novel zebrafish xenograft model in ache mutants using liver cancer cell lines.Scientific reports · 2018Article
- Fishing for cures: The alLURE of using zebrafish to develop precision oncology therapies.NPJ precision oncology · 2017Article
- Review
- Ultrastructural Mapping of the Zebrafish Gastrointestinal System as a Basis for Experimental Drug Studies.BioMed research international · 2016Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here we report a new transgenic expression system by combination of liver-specific expression, mifepristone induction and Cre-loxP recombination to conditionally control the expression of oncogenic kras(V12). This transgenic system allowed expression of kras(V12) specifically in the liver by a brief exposure of mifepristone to induce permanent genomic recombination mediated by the Cre-loxP system. We found that liver tumors were generally induced from multiple foci due to incomplete Cre-loxP recombination, thus mimicking naturally occurring human tumors resulting from one or a few mutated cells and clonal proliferation to form nodules. Similar to our earlier studies by both constitutive and inducible expression of the kras(V12) oncogene, hepatocellular carcinoma (HCC) is the main type of liver tumor induced by kras(V12) expression. Moreover, mixed tumors with hepatocellular adenoma and hepatoblastoma (HB) were also frequently observed. Molecular analyses also indicated similar increase of phosphorylated ERK1/2 in all types of liver tumors, but nuclear localization of β-catenin, a sign of malignant transformation, was found only in HCC and HB. Taken together, our new transgenic system reported in this study allows transgenic kras(V12) expression specifically in the zebrafish liver only by a brief exposure of mifepristone to induce permanent genomic recombination mediated by the Cre-loxP system.
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