中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model

文献类型:期刊论文

作者Gong, Zhiyuan5,6; Sun, Yuxi1,5; Lin, Yueh-Min2,3; Lu, Jeng-Wei4,5
刊名ACTA HISTOCHEMICA
出版日期2025-09-01
卷号127期号:3页码:8
关键词Doxycycline Gankyrin Hyperplasia Hepatocellular carcinoma Zebrafish
ISSN号0065-1281
DOI10.1016/j.acthis.2025.152280
通讯作者Lu, Jeng-Wei(lujengwei@mail.ntou.edu.tw)
英文摘要Background: Hepatocarcinogenesis is a complex, multistep process that begins with fatty liver, progresses to fibrosis, and ultimately leads to cancer. Numerous etiological factors contribute to this progression, highlighting the importance of developing animal models to facilitate both basic and translational research aimed at discovering new therapeutic strategies. Gankyrin is a key oncoprotein involved in the genetic regulation of liver pathology. Material and method: To investigate its oncogenic role without the need for cancer cell inoculation or drug treatment, we employed a Tet-On system to drive zebrafish gankyrin overexpression in hepatocytes under the control of the fabp10a promoter. Results: After eight weeks of induction, fabp10a:eGFP-gankyrin transgenic zebrafish spontaneously developed persistent hyperplasia, bile duct hyperplasia, and hepatocellular carcinoma (HCC), demonstrating the oncogenic potential of gankyrin in liver tumorigenesis. In this study, we demonstrate that gankyrin activation drives the progressive development of HCC in zebrafish. Liver-specific overexpression of gankyrin in wild-type zebrafish led to hyperplasia, bile duct hyperplasia, and HCC, establishing a robust zebrafish model for studying liver cancer. Our findings highlight the utility of this model for investigating the molecular mechanisms underlying tumorigenesis. Conclusion: This study establishes a robust zebrafish model in which liver-specific overexpression of gankyrin induces spontaneous progression from hyperplasia to hepatocellular carcinoma. The model provides a valuable platform for investigating the molecular mechanisms of hepatocarcinogenesis and exploring potential therapeutic strategies.
WOS关键词ONCOPROTEIN GANKYRIN ; HEPATOCELLULAR-CARCINOMA ; IN-VIVO ; EXPOSURE ROUTES ; GENE-EXPRESSION ; CANCER ; P53 ; PROTEIN ; TUMORIGENESIS ; DEGRADATION
资助项目Ministry of Education, Singapore[R154000B88112] ; Ministry of Education, Singapore[R154000B70114]
WOS研究方向Cell Biology
语种英语
WOS记录号WOS:001544836600001
出版者ELSEVIER GMBH
源URL[http://ir.qdio.ac.cn/handle/337002/202761]  
专题中国科学院海洋研究所
通讯作者Lu, Jeng-Wei
作者单位1.Southern Univ Sci & Technol, Dept Biol, Shenzhen, Peoples R China
2.Changhua Christian Hosp, Dept Pathol, Changhua, Taiwan
3.Chung Shan Med Univ, Sch Med, Taichung, Taiwan
4.Natl Taiwan Ocean Univ, Dept Biosci & Biotechnol, 2 Beining Rd, Keelung, Taiwan
5.Natl Univ Singapore, Dept Biol Sci, Singapore, Singapore
6.Chinese Acad Sci, Inst Oceanol, Qingdao, Peoples R China
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GB/T 7714
Gong, Zhiyuan,Sun, Yuxi,Lin, Yueh-Min,et al. Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model[J]. ACTA HISTOCHEMICA,2025,127(3):8.
APA Gong, Zhiyuan,Sun, Yuxi,Lin, Yueh-Min,&Lu, Jeng-Wei.(2025).Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model.ACTA HISTOCHEMICA,127(3),8.
MLA Gong, Zhiyuan,et al."Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model".ACTA HISTOCHEMICA 127.3(2025):8.

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来源:海洋研究所

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