期刊文献+
任意字段
题名或关键词
题名
关键词
文摘
作者
第一作者
机构
刊名
分类号
参考文献
作者简介
基金资助
栏目信息

p16在HBsAg和HBx转基因小鼠肝脏肿瘤中的表达

Expression of p16 in Hepatocellular Carcinoma of HBsAg and HBx Transgenic Mice
下载PDF
导出
摘要 目的:探讨p16基因在由乙型肝炎病毒基因整合引起的小鼠肝细胞癌发生发展中的表达变化规律。方法:以乙肝病毒表面抗原基因(HBsAg)及X基因(HBx)定位整合转基因小鼠及对照小鼠的肝脏组织为标本,利用North-ern印迹、Western印迹及免疫组织化学检测p16在乙肝病毒基因定位整合转基因小鼠肝脏正常组织与肿瘤组织中的差异表达。结果:p16主要在小鼠胚胎期的肝脏中表达,在新生小鼠和成年小鼠的肝脏组织中几乎检测不到其表达;在HBsAg转基因小鼠和HBx转基因小鼠的肝脏肿瘤中,p16的表达明显升高。结论:p16基因在HBsAg或HBx诱导的肝细胞癌发生过程中被重新激活,也许发挥重要的作用。 Objective： To study the expression of p16 in the process of HBV-related hepatocarcinogenesis.Methods： The expression of p16 in liver tissues and tumors of HBsAg and HBx transgenic mice and wild type control mice was evaluated by Northern blot,Western blot and immunohistochemical analysis.Results： p16 expression was detected in fetal liver,but barely detected in liver of control mice after birth.The expression of p16 was up-regulated in liver tumors of HBsAg and HBx transgenic mice when compared with adjacent normal tissues.Conclusion： p16 was reactivated,and might have important function during the process of HBV-related hepatocarcinogenesis.
作者 孙耀兰 赵士林 侯宁 王丽娟 王友亮 杨晓
机构地区 军事医学科学院生物工程研究所蛋白质组学国家重点实验室
出处 《生物技术通讯》 CAS 2012年第1期30-33,共4页 Letters in Biotechnology
基金 国家重大科学研究计划(2011CB910601)
关键词 乙型肝炎病毒 转基因小鼠 肝细胞癌 P16基因 hepatitis B virus transgenic mice hepatocellular carcinoma p16 gene
分类号 R730 [医药卫生—肿瘤] Q789 [生物学—分子生物学]
  • 相关文献

参考文献20

  • 1Libbrecht L,Desmet V,Roskams T.Preneoplastic lesions inhuman hepatocarcinogenesis[J].Liver Int,2005,25(1):16-27.
  • 2Roncalli M,Borzio M,Di Tommaso L.Hepatocellular dysplas-tic nodules[J].Ann Ital Chir,2008,79(2):81-89.
  • 3Bosch F X,Ribes J,Borras J.Epidemiology of primary livercancer[J].Semin Liver Dis,1999,19(3):271-285.
  • 4Wang Y,Cui F,Lv Y,et al.HBsAg and HBx knocked intothe p21 locus causes hepatocellular carcinoma in mice[J].Hepatology,2004,39(2):318-324.
  • 5Cui F,Wang Y,Wang J,et al.The up-regulation of protea-some subunits and lysosomal proteases in hepatocellular carci-nomas of the HBx gene knockin transgenic mice[J].Proteomics,2006,6(2):498-504.
  • 6Vidal A,Koff A.Cell-cycle inhibitors:three families united bya common cause[J].Gene,2000,247(1-2),1-15.
  • 7Nishida N,Nagasaka T,Nishimura T,et al.Aberrant methyla-tion of multiple tumor suppressor genes in aging liver,chronichepatitis,and hepatocellular carcinoma[J].Hepatology,2008,47(3):908-918.
  • 8Sherr C J.Cancer cen cycles[J].Science,1996,274(5293):1672-1677.
  • 9Narimatsu T,Tamori A,Koh N,et al.p16 promoter hyperme-thylation in human hepatocellular carcinoma with or withouthepatitis virus infection[J].Intervirology,2004;47(1):26-31.
  • 10王影,杨素琼,王在国,蒲晓东,孙维纲,刘光中.原发性肝细胞癌组织中P16蛋白表达的意义[J].华人消化杂志,1998,6(5):412-414. 被引量：8

二级参考文献12

  • 1Tannapfel A, Wasner M, Krause K, et al. Expression of p73 and its relation to histopathology and prognosis in hepatocellular carcinoma[J]. J Nail Cancer Inst, 1999, 91(13): 1154-1158.
  • 2Herath NI, Kew MC, Whitehall VLJ, et al. p73 is up-regulated in a subset of hepatocellular carcinoma[J]. Hepatology, 2000,31 (3): 601 - 605.
  • 3Qin LF, Ng IO. Expression of p27(KIPI) and p21(WAF1/CIP1) in primary hepatocellular carcinoma: clinicopathologic correlation and survival analysis[J]. Hum Pathol, 2001, 21 (8):778 - 784.
  • 4Ito Y, Takeda T, Sakon M, et al. Expression of p57/kip2 protein in hepatocellular carcinoma[J]. Oncology, 2001,61 (3):221 - 225.
  • 5Obata M, Imamura E, Yoshida Y, et al. Resistance of primary cultured mouse hepatic tumor cells, cellular senescence despite expression of pl6(Ink4a), p19(Arf), p53 and p21 (wafl/cipl )[J]. Mol Carcinog, 2001,32(1):9- 18.
  • 6Silins I, Finnberg N, Stahl A, et al. Reduced ATM kinase activity and an attenuated p53 response to DNA damage in carcinogen-induced preneoplastic hepatic lesions in the rat[J].Carcinogenesis, 2001, 22 (12) : 2023 - 2031.
  • 7Garkavtsev I, Kazarov A, Gudkov A, et al. Suppression of the novel growth inhibitor p33^INGI promotes neplastic transformation[J]. Nature Genet, 1996, 14(4):415 -420.
  • 8Pandita TK. ATM function and telomere stability[J]. Oncogene,2002, 21 (4): 611 -618.
  • 9Zhu J, Jiang J, Zhou W, et al. The potential tumor suppressor p73 differentially regulates cellular p53 target genes[J]. Cancer Res, 1998, 58 (22) : 5061 - 5065.
  • 10Zeng X, Chen L, Jost CA, et al. MDM2 suppresses p73 function without promoting p73 degradation[J]. Mol Cell Biol, 1999, 19(5): 3257 - 3266.

共引文献20

生物技术通讯
2012年 第1期

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部