Research Advances on the Applications of Hepatocellular Carcinoma Transgenic Mouse Models

doi:10.13560/j.cnki.biotech.bull.1985.2015.12.008

Abstract

Abstract: Hepatocellular carcinoma(HCC)is one of the most malignant tumors worldwide. Due to the rapid progress of HCC and the high rate of recurrence and metastasis, the early diagnosis and efficient treatment have been the challenging issues in clinic, and the etiopathogenesis of HCC urgently needs further being clarified. Transgenic mouse models established by genetic engineering provide important research platforms for the etiopathogenesis and drug screening of liver cancer. Combing the classic researches and recent advances, the construction and characteristics of commonly used HCC transgenic mouse models, especially the applications of these transgenic models in HCC basic researches are classified, moreover the developmental prospects of this field are also included.

Key words: hepatocellular carcinoma(HCC), transgenic, mouse model

Zhao Yinghua, Sun Wei. Research Advances on the Applications of Hepatocellular Carcinoma Transgenic Mouse Models[J]. Biotechnology Bulletin, 2015, 31(12): 56-62.

References

[1] Stewart BW, Wild CP. World cancer report 2014[C]. International Agency for Research on Cancer, 2014.
[2] Gordon JW, Ruddle FH. Germ line transmission in transgenic mice[J]. Progress in Clinical and Biological Research, 1981, 85:111-124.
[3] Koike K, Moriya K, Iino S, et al. High-level expression of hepatitis B virus HBx gene and hepatocarcinogenesis in transgenic mice[J]. Hepatology, 1994, 19(4):810-819.
[4] 吴一迁, 仇效坤. HBVx 转基因小鼠肝组织基因表达谱的微阵列研究[J]. 肿瘤, 2001, 21(4):235-238.
[5] Madden CR, Finegold MJ, Slagle BL. Hepatitis B virus X protein acts as a tumor promoter in development of diethylnitrosamine-induced preneoplastic lesions[J]. J Virol, 2001, 75(8):3851-3858.
[6] Pollicino T, Terradillos O, Lecoeur H, et al. Pro-apoptotic effect of the hepatitis B virus X gene[J]. Biomed Pharmacother, 1998, 52(9):363-368.
[7] Yu Z, Gao YQ, Feng H, et al. Cell cycle-related kinase mediates viral-host signalling to promote hepatitis B virus-associated hepatocarcinogenesis[J]. Gut, 2014, 63(11):1793-1804.
[8] Quétier I, Brezillon N, Duriez M, et al. Hepatitis B virus HBx protein impairs liver regeneration through enhanced expression of IL-6 in transgenic mice[J]. J Hepatol, 2013, 59(2):285-291.
[9] Wu YF, Fu SL, Kao CH, et al. Chemopreventive effect of silymarin on liver pathology in HBV X protein transgenic mice[J]. Cancer Res, 2008, 68(6):2033-2042.
[10] Yamazaki K, Suzuki K, Ohkoshi S, et al. Temporal treatment with interferon-Β prevents hepatocellular carcinoma in hepatitis B virus X gene transgenic mice[J]. J Hepatol, 2008, 48(2):255-265.
[11] Chisari FV, Klopchin K, Moriyama T, et al. Molecular pathogenesis of hepatocellular carcinoma in hepatitis B virus transgenic mice[J]. Cell, 1989, 59(6):1145-1156.
[12] Koike K, Moriya K, Kimura S. Role of hepatitis C virus in the development of hepatocellular carcinoma:transgenic approach to viral hepatocarcinogenesis[J]. J Gastroenterol Hepatol, 2002, 17(4):394-400.
[13] Kamegaya Y, Hiasa Y, Zukerberg L, et al. Hepatitis C virus acts as a tumor accelerator by blocking apoptosis in a mouse model of hepatocarcinogenesis[J]. Hepatology, 2005, 41(3):660-667.
[14] Benzoubir N, Lejamtel C, Battaglia S, et al. HCV core-mediated activation of latent TGF-Β via thrombospondin drives the crosstalk between hepatocytes and stromal environment[J]. J Hepatol, 2013, 59(6):1160-1168.
[15] Fujinaga H, Tsutsumi T, Yotsuyanagi H, et al. Hepatocarcinogenesis in hepatitis C:HCV shrewdly exacerbates oxidative stress by modulating both production and scavenging of reactive oxygen species[J]. Oncology, 2011, 81(Suppl. 1):11-17.
[16] Lou D Q, Molina T, Bennoun M, et al. Conditional hepatocarcinoge-nesis in mice expressing SV 40 early sequences[J]. Cancer Lett, 2005, 229(1):107-114.
[17] Colvin EK, Weir C, Ikin RJ, et al. SV40 TAg mouse models of cancer[C]. Seminars in Cell & Developmental Biology. Academic Press, 2014, 27:61-73.
[18] Runge A, Hu J, Wieland M, et al. An inducible hepatocellular carcinoma model for preclinical evaluation of anti-angiogenic therapy in adult mice[J]. Cancer Res, 2014, 74(15):4157-4169.
[19] Willimsky G, Schmidt K, Loddenkemper C, et al. Virus-induced hepatocellular carcinomas cause antigen-specific local tolerance[J]. J Clin Invest, 2013, 123(3):1032-1043.
[20] Boissan M, Wendum D, Arnaud-Dabernat S, et al. Increased lung metastasis in transgenic NM23-Null/SV40 mice with hepatocellular carcinoma[J]. J Natl Cancer Inst, 2005, 97(11):836-845.
[21] Nambotin SB, Lefrancois L, Sainsily X, et al. Pharmacological inhibition of Frizzled-7 displays anti-tumor properties in hepatoce-llular carcinoma[J]. J Hepatol, 2011, 54(2):288-299.
[22] Lee JS, Chu IS, Mikaelyan A, et al. Application of comparative functional genomics to identify best-fit mouse models to study human cancer[J]. Nat Genet, 2004, 36(12):1306-1311.
[23] Santoni-Rugiu E, Nagy P, Jensen MR, et al. Evolution of neoplastic development in the liver of transgenic mice co-expressing c-myc and transforming growth factor-alpha[J]. Am J Pathol, 1996, 149(2):407-428.
[24] Conner EA, Lemmer ER, Sánchez A, et al. E2F1 blocks and c-Myc accelerates hepatic ploidy in transgenic mouse models[J]. Biochem Biophys Res Commun, 2003, 302(1):114-120.
[25] Srivastava J, Siddiq A, Gredler R, et al. Astrocyte elevated gene-1(AEG-1)and c-Myc cooperate to promote hepatocarcinogenesis[J]. Hepatology, 2015, 61(3):915-929.
[26] Harada N, Oshima H, Katoh M, et al. Hepatocarcinogenesis in mice with Β-catenin and Ha-ras gene mutations[J]. Cancer Res, 2004, 64(1):48-54.
[27] Stauffer JK, Scarzello AJ, Andersen JB, et al. Coactivation of AKT and Β-catenin in mice rapidly induces formation of lipogenic liver tumors[J]. Cancer Res, 2011, 71(7):2718-2727.
[28] Dong B, Lee JS, Park YY, et al. Activating CAR and Β-catenin induces uncontrolled liver growth and tumorigenesis[J]. Nat Commun, 2015, 6:5944.
[29] Borlak J, Meier T, Halter R, et al. Epidermal growth factor-induced hepatocellular carcinoma:gene expression profiles in precursor lesions, early stage and solitary tumors[J]. Oncogene, 2005, 24(11):1809-1819.
[30] Liedtke C, Zschemisch NH, Cohrs A, et al. Silencing of caspase-8 in murine hepatocellular carcinomas is mediated via methylation of an essential promoter element[J]. Gastroenterology, 2005, 129(5):1602-1615.
[31] Gazzana G, Borlak J. Mapping of the serum proteome of hepatocellular carcinoma induced by targeted overexpression of epidermal growth factor to liver cells of transgenic mice[J]. J Proteome Res, 2008, 7(3):928-937.
[32] Watanabe S, Horie Y, Kataoka E, et al. Non-alcoholic steatohepatitis and hepatocellular carcinoma:Lessons from hepatocyte-specific phosphatase and tensin homolog(PTEN)-deficient mice[J]. J Gastroenterol Hepatol, 2007, 22(s1):S96-S100.
[33] Xue W, Chen S, Yin H, et al. CRISPR-mediated direct mutation of cancer genes in the mouse liver[J]. Nature, 2014, 514(7522):380-384.
[34] Heindryckx F, Colle I, Van Vlierberghe H. Experimental mouse models for hepatocellular carcinoma research[J]. Int J Exp Pathol, 2009, 90(4):367-386.
[35] Koo JS, Seong JK, Park C, et al. Large liver cell dysplasia in hepatitis B virus X transgenic mouse liver and human chronic hepatitis B virus-infected liver[J]. Intervirology, 2005, 48(1):16-22.
[36] Zheng YY, Chen WL, Louie SG, et al. Hepatitis B virus promotes hepatocarcinogenesis in transgenic mice[J]. Hepatology, 2007, 45(1):16-21.
[37] Lau CC, Sun T, Ching AKK, et al. Viral-human chimeric transcript predisposes risk to liver cancer development and progression[J]. Cancer Cell, 2014, 25(3):335-349.
[38] Tanaka N, Moriya K, Kiyosawa K, et al. Hepatitis C virus core protein induces spontaneous and persistent activation of peroxisome proliferator-activated receptor α in transgenic mice:Implications for HCV-associated hepatocarcinogenesis[J]. Int J Cancer, 2008, 122(1):124-131.
[39] Nevzorova YA, Hu W, Cubero FJ, et al. Overexpression of c-myc in hepatocytes promotes activation of hepatic stellate cells and facilitates the onset of liver fibrosis[J]. Biochim Biophys Acta, 2013, 1832(10):1765-1775.
[40] Griffitts J, Tesiram Y, Reid GE, et al. In vivo MRS assessment of altered fatty acyl unsaturation in liver tumor formation of a TGFα/c-myc transgenic mouse model[J]. J Lipid Res, 2009, 50(4):611-622.
[41] Coulouarn C, Factor VM, Conner EA, et al. Genomic modeling of tumor onset and progression in a mouse model of aggressive human liver cancer[J]. Carcinogenesis, 2011, 32(10):1434-1440.
[42] Tward AD, Jones KD, Yant S, et al. Distinct pathways of genomic progression to benign and malignant tumors of the liver[J]. Proc Natl Acad Sci USA, 2007, 104(37):14771-14776.
[43] Wang R, Ferrell LD, Faouzi S, et al. Activation of the Met receptor by cell attachment induces and sustains hepatocellular carcinomas in transgenic mice[J]. J Cell Biol, 2001, 153(5):1023-1034.
[44] Rogler CE, Yang D, Rossetti L, et al. Altered body composition and increased frequency of diverse malignancies in insulin-like growth factor-II transgenic mice[J]. J Biol Chem, 1994, 269(19):13779-13784.
[45] Nicholes K, Guillet S, Tomlinson E, et al. A mouse model of hepatocellular carcinoma:ectopic expression of fibroblast growth factor 19 in skeletal muscle of transgenic mice[J]. Am J Pathol, 2002, 160(6):2295-2307.
[46] Okada H, Honda M, Campbell JS, et al. Acyclic retinoid targets platelet-derived growth factor signaling in the prevention of hepatic fibrosis and hepatocellular carcinoma development[J]. Cancer Res, 2012, 72(17):4459-4471.
[47] Martínez-Chantar ML, Vázquez-Chantada M, Ariz U, et al. Loss of the glycine N-methyltransferase gene leads to steatosis and hepatocellular carcinoma in mice[J]. Hepatology, 2008, 47(4):1191-1199.
[48] Li Y, Tang ZY, Hou JX. Hepatocellular carcinoma:insight from animal models[J]. Nat Rev Gastroenterol Hepatol, 2012, 9(1):32-43.
[49] Bakiri L, Wagner EF. Mouse models for liver cancer[J]. Mol Oncol, 2013, 7(2):206-223.