斑马鱼作为肝癌模型的应用进展

王新娟

doi:10.3969/j.issn.1001-5256.2016.07.049

斑马鱼作为肝癌模型的应用进展

DOI: 10.3969/j.issn.1001-5256.2016.07.049

王新娟

西南大学生命科学学院

详细信息

中图分类号: R735.7;R-332
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出版历程
- 出版日期: 2016-07-20

Research advances in zebrafish as a model of liver cancer

Wang XinJuan

摘要

摘要: 近年来,肝癌的发病率呈上升趋势,进一步了解肝癌发生的相关分子机制,了解其致病机理,对保障健康有重要意义。斑马鱼是一种重要的模式生物,与人类基因高度保守,其生长速度快,早期胚胎透明,有助于对发育过程实时观测;并且其肝脏细胞的构成、功能、信号通路,甚至是对于损伤的反应都与人类极度相似。在现代生物研究中,斑马鱼作为人类肝病模型得到广泛应用。主要介绍了斑马鱼作为肝癌模型的应用及研究进展,认为斑马鱼肝癌模型构建技术已经较为成熟,随着实验技术的不断发展,其在肝癌研究领域将取得更大的进步。
- 肝肿瘤,实验性 /
- 斑马鱼 /
- 综述
Abstract: The incidence rate of liver cancer tends to increase in recent years,and the molecular and pathogenic mechanisms of liver cancer should be further investigated to guarantee health. As an important model organism,zebrafish have highly conserved genes and grow fast.The early embryo of zebrafish is transparent,which helps with the real- time observation of the development process. Zebrafish are similar to humans in the composition,function,and signaling pathways of hepatocytes,as well as response to injury. In modern biological studies,zebrafish have been wildly used as the model of liver diseases. This article summarizes the research advances in the application of zebrafish as the model of liver cancer,and points out that the techniques for establishing the zebrafish model of liver cancer have become mature. With the constant development of experimental techniques,great achievements will be achieved in the field of liver cancer.
- liver neoplasms /
- experimental /
- zebrafish

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参考文献(32)

[1]ZHENG RS,ZUO TT,ZENG HM,et al.Mortality and survival analysis of liver cancer in China[J].Chin J Oncol,2015,37(9):697-702.(in Chinese)郑荣寿,左婷婷,曾红梅,等.中国肝癌死亡状况与生存分析[J].中华肿瘤杂志,2015,37(9):697-702.

[2]ZUO TT,ZHENG RS,ZENG HM,et al.Analysis of liver cancer incidence and trend in China[J].Chin J Oncol,2015,37(9):691-696.(in Chinese)左婷婷,郑荣寿,曾红梅,等.中国肝癌发病状况与趋势分析[J].中华肿瘤杂志,2015,37(9):691-696.

[3]LI L,BONNETON F,TOHME M,et al.In vivo screening using transgenic zebrafish embryos reveals new effects of HDAC inhibitors trichostatin A and valproic acid on organogenesis[J].PLoS One,2016,11(2):e0149497.

[4]FARMEN E,HULTMAN MT,ANGLS D'AURIAC M,et al.Development of a screening system for the detection of chemically induced DNA methylation alterations in a zebrafish liver cell line[J].J Toxicol Environ Health A,2014,77(9-11):587-599.

[5]LIN TY,CHOU CF,CHUNG HY,et al.Hypoxia-inducible factor 2 alpha is essential for hepatic outgrowth and functions via the regulation of leg1 transcription in the zebrafish embryo[J].PLoSOne,2014,9(7):e101980.

[6]SPITSBERGEN JM,TSAI HW,REDDY A,et al.Neoplasia in zebrafish(Danio rerio)treated with 7,12-dimethylbenz[a]-anthracene by two exposure routes at different developmental stages[J].Toxicol Pathol,2000,28(5):705-715.

[7]LU JW,YANG WY,TSAI SM,et al.Liver-specific expressions of HBx and src in the p53 mutant trigger hepatocarcinogenesis in zebrafish[J].PLoS One,2013,8(10):e76951.

[8]SUN L,NGUYEN AT,SPITSBERGEN JM,et al.Myc-induced liver tumors in transgenic zebrafish can regress in tp53 null mutation[J].PLoS One,2015,10(1):e0117249.

[9]HARAMIS AP,HURLSTONE A,van der VELDEN Y,et al.Adenomatous polyposis coli-deficient zebrafish are susceptible to digestive tract neoplasia[J].EMBO Rep,2006,7(4):444-449.

[10]EVASON KJ,FRANCISCO MT,JURIC V,et al.Identification of chemical inhibitors ofβ-catenin-driven liver tumorigenesis in zebrafish[J].PLoS Genet,2015,11(7):e1005305.

[11]NGUYEN AT,KOH V,SPITSBERGEN JM,et al.Development of a conditional liver tumor model by mifepristone-inducible Cre recombination to control oncogenic kras(V12)expression in transgenic zebrafish[J].Sci Rep,2016,6:19559.

[12]YAN C,HUO X,WANG S,et al.Stimulation of hepatocarcinogenesis by neutrophils upon induction of oncogenic kras expression in transgenic zebrafish[J].J Hepatol,2015,63(2):420-428.

[13]CHEW TW,LIU XJ,LIU L,et al.Crosstalk of Ras and Rho:activation of RhoA abates Kras-induced liver tumorigenesis in transgenic zebrafish models[J].Oncogene,2014,33(21):2717-2727.

[14]LI Z,ZHENG W,LI H,et al.Synergistic induction of potential warburg effect in zebrafish hepatocellular carcinoma by co-transgenic expression of myc and xmrk oncogenes[J].PLoS One,2015,10(7):e0132319.

[15]LI Z,LUO H,LI C,et al.Transcriptomic analysis of a transgenic zebrafish hepatocellular carcinoma model reveals a prominent role of immune responses in tumour progression and regression[J].Int JCancer,2014,135(7):1564-1573.

[16]ZHENG W,LI Z,NGUYEN AT,et al.Xmrk,kras and myc transgenic zebrafish liver cancer models share molecular signatures with subsets of human hepatocellular carcinoma[J].PLoS One,2014,9(3):e91179.

[17]CUI J,SIM TH,GONG Z,et al.Generation of transgenic zebrafish with liver-specific expression of EGFP-Lc3:a new in vivo model for investigation of liver autophagy[J].Biochem Biophys Res Commun,2012,422(2):268-273.

[18]JENSEN LD.The circadian clock and hypoxia in tumor cell de-differentiation and metastasis[J].Biochim Biophys Acta,2015,1850(8):1633-1641.

[19]OEHLERS SH,CRONAN MR,SCOTT NR,et al.Interception of host angiogenic signalling limits mycobacterial growth[J].Nature,2015,517(7536):612-615.

[20]ELKS PM,RENSHAW SA,MEIJER AH,et al.Exploring the HIFs,buts and maybes of hypoxia signalling in disease:lessons from zebrafish models[J].Dis Model Mech,2015,8(11):1349-1360.

[21]BRUTIGAM L,PUDELKO L,JEMTH AS,et al.Hypoxic signaling and the cellular redox tumor environment determine sensitivity to MTH1inhibition[J].Cancer Res,2016,76(8):2366-2375.

[22]SANTHAKUMAR K,JUDSON EC,ELKS PM,et al.A zebrafish model to study and therapeutically manipulate hypoxia signaling in tumorigenesis[J].Cancer Res,2012,72(16):4017-4027.

[23]SINGLETON DC,ROUHI P,ZOIS CE,et al.Hypoxic regulation of RIOK3 is a major mechanism for cancer cell invasion and metastasis[J].Oncogene,2015,34(36):4713-4722.

[24]KREMER-TAL S,REEVES HL,NARLA G,et al.Frequent inactivation of the tumor suppressor Krüppel-like factor 6(KLF6)in hepatocellular carcinoma[J].Hepatology,2004,40(5):1047-1052.

[25]LANG UE,KOCABAYOGLU P,CHENG GZ,et al.GSK3βphosphorylation of the KLF6 tumor suppressor promotes its transactivation of p21[J].Oncogene,2013,32(38):4557-4564.

[26]DIAB T,HANOUN N,BUREAU C,et al.The Role of the 3'untranslated region in the post-transcriptional regulation of KLF6gene expression in hepatocellular carcinoma[J].Cancers(Basel),2013,6(1):28-41.

[27]LIANG WC,WANG Y,XIAO LJ,et al.Identification of miRNAs that specifically target tumor suppressive KLF6-FL rather than oncogenic KLF6-SV1 isoform[J].RNA Biol,2014,11(7):845-854.

[28]ZHAO X,MONSON C,GAO C,et al.Klf6/copeb is required for hepatic outgrowth in zebrafish and for hepatocyte specification in mouse ES cells[J].Dev Biol,2010,344(1):79-93.

[29]ABE H,OGAWA T,WANG L,et al.Promoter-region hypermethylation and expression downregulation of Yy1(Yin yang 1)in preneoplastic liver lesions in a thioacetamide rat hepatocarcinogenesis model[J].Toxicol Appl Pharmacol,2014,280(3):467-474.

[30]SHAN X,REN M,CHEN K,et al.Regulation of the microRNA processor DGCR8 by hepatitis B virus proteins via the transcription factor YY1[J].Arch Virol,2015,160(3):795-803.

[31]YE SL.Current challenges to primary liver cancer research[J].JClin Hepatol,2015,31(6):819-823.(in Chinese)叶胜龙.原发性肝癌研究当前面临的挑战[J].临床肝胆病杂志,2015,31(6):819-823.

[32]DENG X,WU JB.Updates in the research of relationship between MicroRNAs and hepatocellular carcinoma[J].Chin J Dig Surg,2015,14(5):431-433.(in Chinese)邓曦,吴敬波.微RNAs与肝癌关系的研究进展[J].中华消化外科杂志,2015,14(5):431-433.

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