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p14^(ARF)、ARF-BP1及c-myc mRNA在肝细胞癌中的表达及临床意义 被引量:1

Expression of p14^(ARF),ARF-BP1 and c-myc mRNAs in hepatocellular carcinoma and their significances
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摘要 目的:探讨肝细胞癌组织中p14ARF、ARF-BP1及c-myc的mRNA表达及其与临床参数关系.方法:采用半定量逆转录-聚合酶链式反应(RT-PCR)技术,对52例HCC组织及其中45例相应癌旁组织p14ARF、ARF-BP1及c-myc的mRNA表达丰度进行检测并分析他们之间的关系及其与临床参数的关系.结果:在52例HCC组织中p14ARF、ARF-BP1及c-myc的mRNA各表达77.0%、77.0%和75.0%,与45例相应癌旁组织(11.1%、20.0%、53.3%)比较,呈高表达.p14ARF、ARF-BP1mRNA的表达与肿瘤大小有关(t=2.169,2.087,均P<0.05);而c-mycmRNA表达与肿瘤大小无关.p14ARF、ARF-BP1及c-myc的mRNA表达在性别、年龄、AFP、临床病理分级、浸润转移、HBV、包膜等无统计学差异.p14ARF与ARF-BP1、p14ARF与c-myc及ARF-BP1与c-myc的mRNA表达两两成正相关(r=0.565,0.436,0.584,均P<0.01).结论:p14ARF、ARF-BP1、c-myc过度表达可能是HCC发生的早期指标;ARF-BP1过度表达可能是影响HCC发生、发展的关键,干预ARF-BP1可能是治疗HCC的新途径. AIM: To investigate the expression of p14^ARF, ARF-BP1 and c-myc mRNAs in hepatocellular carcinoma (HCC) and their clinical significances. METHODS: Abundance of p14^ARF, ARF-BP1 and c-myc mRNAs was detected by semi-quantification reverse transcription polymerase chain reaction (RT-PCR) technique in the samples from 52 HCCs and their 45 non-tumorous liver tissues, and their clinical significances were assayed with the clinical parameters. RESULTS: The expression levels of p14^ARF, ARF-BP1 and c-myc mRNAs (77.0%, 77.0%, 75.0%) were higher in HCC tissues than those in the non-tumorous liver tissues (11.1%, 20.0%, 53.3%), respectively. The expression of p14^ARF mRNA and ARF-BP1 mRNAs were related to tumor size (t = 2.169, 2.087; both P 〈 0.05), but the expression of c-myc mRNA was not. The expression of p14^ARF, ARF-BP1 and c-myc mRNAs were not related to the gender, age, AFP level, clinical stageing, HBV infection, envelopes, infiltration and metastasis. There was a positive correlation between p14^ARF and ARF-BP1 expression, p14^ARF and c-myc expression as well as ARF-BP1 and c-myc expression (r = 0.565, 0.436, 0.584; all P 〈 0.01). CONCLUSION: Over-expression of p14^ARF, ARF- BP1 and c-myc mRNAs are markers in the early stage of HCC, and ARF-BP1 over-expression play an important role in the genesis and development of HCC, ARF-BP1 may become a novel therapeutic target against HCC.
出处 《世界华人消化杂志》 CAS 北大核心 2008年第23期2656-2660,共5页 World Chinese Journal of Digestology
基金 广西自然科学基金资助项目 No.桂科自0542071 广西科学研究与技术开发计划资助项目 No.桂科能05112001-4D~~
关键词 p14^ARF^ ARF-BP1 C-MYC 肝细胞癌 逆转录-聚合酶链式反应 p14^ARF ARF-BP1 c-myc Hepatocellular carcinoma Reverse transcription polymerase chain reaction
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  • 1Chen C, Matesic LE. The Nedd4-like family of E3 ubiquitin ligases and cancer. Cancer Metastasis Rev 2007; 26: 587-604
  • 2Chen D, Kon N, Li M, Zhang W, Qin J, Gu W. ARF-BP1/Mule is a critical mediator of the ARF tumor suppressor. Cell 2005; 121: 1071-1083
  • 3Adhikary S, Marinoni F, Hock A, Hulleman E, Popov N, Beier R, Bernard S, Quarto M, Capra M, Goettig S, Kogel U, Scheffner M, Helin K, Eilers M. The ubiquitin ligase HectH9 regulates transcriptional activation by Myc and is essential for tumor cell proliferation. Cell 2005; 123: 409-421
  • 4Vousden KH. p53: death star. Cell 2000; 103: 691-694
  • 5Tannapfel A, Busse C, Geissler F, Witzigmann H, Hauss J, Wittekind C. INK4a-ARF alterations in liver cell adenoma. Gut 2002; 51: 253-258
  • 6Chang LL, Yeh WT, Yang SY, Wu WJ, Huang CH. Genetic alterations of p16INK4a and p14ARF genes in human bladder cancer. J Urol 2003; 170: 595-600
  • 7Vonlanthen S, Heighway J, Tschan MP, Borner MM, Altermatt HJ, Kappeler A, Tobler A, Fey MF, Thatcher N, Yarbrough WG, Betticher DC. Expression of p16INK4a/p16alpha and p19ARF/p16beta is frequently altered in non-small cell lung cancer and correlates with p53 overexpression. Oncogene 1998; 17: 2779-2785
  • 8Iida S, Akiyama Y, Nakajima T, Ichikawa W, Nihei Z, Sugihara K, Yuasa Y. Alterations and hypermethylation of the p14(ARF) gene in gastric cancer. Int J Cancer 2000; 87: 654-658
  • 9Esteller M, Tortola S, Toyota M, Capella G, Peinado MA, Baylin SB, Herman JG. Hypermethylation-associated inactivation of p14(ARF) is independent of p16(INK4a) methylation and p53 mutational status. Cancer Res 2000; 60: 129-133
  • 10Tannapfel A, Busse C, Weinans L, Benicke M, Katalinic A, Geissler F, Hauss J, Wittekind C. INK4a-ARF alterations and p53 mutations in hepatocellular carcinomas. Oncogene 2001; 20: 7104-7109

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同被引文献11

  • 1Chen D, Brooks CL, Gu W. ARF-BP1 as a potential therapeutic target[ J ]. Br J Cancer, 2006,94 ( 11 ) : 1555-1558.
  • 2Zhang X, Berger FG, Yang J, et al. USP4 inhibits p53 through deubiquitinating and stabilizing ARF-BPI[J]. EMBO J, 2011,30 ( 11 ) :2177-2189.
  • 3Thompson CB. Apoptosis in the pathogenesis and treatment of dis- ease[J]. Science, 1995,267(5203) :1456-1462.
  • 4Cben D, /Con N, Li M, et al. ARF-BP1/Mule is a critical mediator of the ARF tumor suppressor[ J ]. Cell, 2005,121 (7) : 1071-1083.
  • 5Kon N, Zhong J, Qiang L, et al. Inactivation of arf-bpl induces p53 activation and diabetic phenotypes in mice[J]. J Biol Chem, 2012,287(7) :5102-5111.
  • 6Moulding DA, Giles RV, Spiller DG, et al. Apoptosis is rapidly triggered by antisense depletion of MCL-1 in differentiating U937 cells [ J ]. Blood, 2000,96 ( 5 ) : 1756 -1 763.
  • 7Derenne S, Monia B, Dean NM, et al. Antisense strategy shows that Mcl-1 rather than Bcl-2 or Bcl-x(L) is an essential survival protein of human myeloma cells [ J ]. Blood, 2002, 100 ( 1 ) : 194-199.
  • 8Backus HH, van Riel JM, van Groeningen C J, et al. Rb, mcl-1 and p53 expression correlate with clinical outcome in patients with liver metastases from colorectal cancer [ J ]. Ann Oneol, 2001,12 (6) :779-785.
  • 9Sieghart W, Losert D, Strommer S, et al. Mcl-1 overexpression in hepatocellular carcinoma: a potential target for antisense therapy [J]. J Hepatol, 2006,44(1) :151-157.
  • 10Ross A J, Li M, Yu B, et al. The EEL-1 ubiquitin ligase promotes DNA damage-induced germ cell apoptosis in C. elegans [ J ]. Cell Death Differ, 2011,18(7) :1140-1149.

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