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SOCS1与c-myc在人肝细胞癌组织中的表达及相互关系 被引量:1

Expressions and relationship of suppressor of cytokine signaling1 and c-myc in human hepatocellular carcinoma tissue
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摘要 目的:研究细胞因子信号转导抑制因子1(SOCS1)和原癌基因c-myc在肝细胞癌(HCC)组织中的表达及二者在HCC中的相互作用。方法:应用免疫组织化学技术检测SOCS1蛋白和c-myc蛋白在41例HCC癌组织、癌旁组织和11例正常肝组织中的表达;采用RT-PCR技术检测上述组织中SOCS1mRNA的表达水平;分析临床、病理资料。结果:HCC癌组织中SOCS1蛋白阳性率和SOCS1mRNA的表达水平明显低于癌旁组织和正常肝组织(P<0.01),SOCS1蛋白在低分化HCC癌组织中的阳性率较高分化HCC癌组织明显减低(P<0.01)。HCC转移组SOCS1蛋白表达阳性率较未转移组低(P<0.05)。HCC癌组织中c-myc蛋白明显高于癌旁组织和正常肝组织;在HCC癌组织中SOCS1蛋白表达强度与c-myc蛋白表达强度呈负相关(P<0.01)。结论:SOCS1在HCC癌组织中表达下调,可能通过一系列途径造成c-myc的激活,从而造成肿瘤的发生。 Objective: To study the expression of suppressor of cytokine signaling 1 (SOCSi) and cellular myelocytomatosis oncogene (c-myc)in hepatocellular Carcinoma (HCC), and to investigate the relation between the expression of SOCS1 and c-myc in HCC. Methods: The expressions of SOCS1 and c-myc protein of 41 HCC tissues and surrounding tissues, as well as the tissues of 11 normal cases, were detected by immunohistochemical (IHC) staining using SP method. The expression of SOCS1 mRNA was detected by RT-PCR. And the clinicai and pathological data were analysed. Results: Compared with the para-carcinoma and normal liver tissue, the levels of SOCS1 and SOCS 1 mRNA in HCC tissues were significantly lower(P〈0.01). Expression of the SOCS1 protein was negatively correlated with pathological degree(P〈0.01). Expression of the SOCS1 protein was reduced in invasive and metastatic HCC tumor, Expression of SOCS1 was negatively corre ated w th expression of c,myc in HCC tissues(P〈0.01). Conclusion: The deactivation Of SOCS1 gene may cause an activation of c-myc gene and eventually lead to hepatocarcinogenesis.
出处 《中国现代普通外科进展》 CAS 2009年第9期765-768,共4页 Chinese Journal of Current Advances in General Surgery
关键词 肝细胞 细胞因子信号转导蛋白抑制因子 原癌基因蛋白质C-MYC Hepotocellular, carcinoma · Suppressor of cytokine signaling Proteins · Proto-oncogene protein c-myc
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  • 1Tan JC, Rabkin R. Suppressors of cytokine signaling in health and disease[J]. Pediatr Nephrol, 2005,20(5):567-575.
  • 2Yoshikawa H, Matsubara K, Qian GS, et al. SOCS-1, a negative regulator of the JAK/STAT pathway, is silenced by methylation in human hepatocellular carcinoma and shows growth-suppression activity[J].Nat Genet, 2001,28(1 ):29-35.
  • 3Friedrich MG, Chandrasoma S, Siegmund KD, et al. Prognostic relevance of methylation markers in patients with non-muscle invasive bladder carcinoma[J]. EurJ Cancer, 2005,41(17):2769-2778.
  • 4Hao XP, Willis JE, Pretlow TG, et al. Loss of ffagigile histidine triad expression in colorectal carcinomas and premalignant lesions [J]. Cancer res, 2000,60( 1 ):18-21.
  • 5Sutherland KD, Lindeman GL, Visder JE, et al. Knocking off SOCS genes in the mammary gland[J].Cell Cycle, 2007,6(7):799-803.
  • 6Hibi K, Nakao A. Highly-methylated colorectal cancers show poorly-differentiated phenotype [J]. Antyicancer Res, 2006,26 (6B): 4263-4266.
  • 7Kyo S, Takakura M, lnoue M. Telornerase activity in caracer as a diagnostic and therapeutic target[J]. Histol Histopathol, 2000,15 ( 3 ):813-824.
  • 8Hemeking H. The MYC oncogene as a cancer drug target[J]. Curt Cancer Drug Targets, 2003,3 (3): 163-175.
  • 9Kiuchi N, Nakajima K, Iehiba M, et al. STAT3 is required for the gp130-mediated full activation of the c-mye gene [J]. J Exp Med, 1999,189 ( 1 ) :63-73.
  • 10Bromberg JF, Darnell JE. Potential roles of Statl and Stat3 in cellular transformation [J]. Cold Spring Harb Syrup Quant Biol, 1999,64:425-428.

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