期刊文献+

肝细胞癌组织Smad4基因表达及其临床意义的研究 被引量:1

Expression of Smad 4 gene in human hepatocellular carcinoma tissues and its significance
原文传递
导出
摘要 目的:拟通过检测Smad4基因在肝细胞癌(HCC)中的表达,初步探讨TGFβ-Smad信号通路中Co-Smad(Smad4)与肝细胞癌的发生和发展之间的可能关系。方法:采用免疫组化ABC法及原位杂交法(ISH)检测41例肝细胞癌组织切片中癌与癌旁Smad4蛋白和mRNA的表达,5例外伤性肝破裂手术切除标本作为正常对照。比较HCC组与对照组及HCC与癌旁Smad4蛋白和mRNA表达的差异,并进行统计分析。结果:正常对照组Smad4蛋白和mRNA均呈阳性表达;HCC组织Smad4蛋白阳性率为48.8%(20/41),癌旁组织中为78.0%(32/41),两者比较差异有统计学意义,P<0.01;HCC组织Smad4mRNA阳性率为51.2%(21/41),癌旁组织中为73.1%(30/41),两者比较差异有统计学意义,P<0.05;与正常肝组织比较,HCC组织中Smad4蛋白和mRNA阳性表达均显著降低,P<0.05;HCC组织Smad4mRNA阳性表达在病理分级Ⅰ、Ⅱ级与Ⅲ、Ⅳ级之间差异有统计学意义,P<0.05。结论:Smad4基因表达缺失可能在肝细胞癌的发生和发展中发挥作用。 OBJECTIVE: To investigate the correlation of Smad4 with carcinogenesis and tumor progression of human hepatocellular carcinoma (HCC). METHODS: ABC and ISH methods were used to detect the expression of Smad4 in 41 casas of HCC, adjacent noncancer liver tissues (ANLT) and 5 mormal controls. The results were processed with T and χ^2 test. RESULT:The expressions of Smad4 and Smad4 mRNA in normal liver tissues were positive. The positive expressions of Smad4 and Smad4 mRNA were detected in 20 cases (48.8%) and 21 cases (51.2%), respectively, for 41 cases of HCC, 32 cases (78.0%) and 30 cases (73.1%) for the corresponding 41 cases of ANLT(P〈0.05). The expression level of Smad4 , as the same as Smad4 mRNA, in HCC tissues was significantly lower than those in ANLT of HCC (P〈0.05). The expression of Smad4 mRNA in HCC tissues was sig nificantly lower in Ⅲ --Ⅳ pathological grades than in Ⅰ-- Ⅱ pathological grades ( P 〈 0.05 ). CONCLUSION: The lower-expression of Smad 4 may play an important role in the occurrence and progression of HCC.
出处 《中华肿瘤防治杂志》 CAS 2009年第3期204-206,共3页 Chinese Journal of Cancer Prevention and Treatment
关键词 肝细胞/遗传学 基因 Smad4 转化生长因子Β 免疫组织化学 carcinoma, hepatocellular genes, Smad4 transforming growth factor beta immunohistochemistry
  • 相关文献

参考文献7

二级参考文献33

  • 1Gressner AM,Weiskirchen R,Breitkopf K,et al.Roles of TGF-beta in hepatic fibrosis[J].Front Biosci,2002;7:d793-d807.
  • 2Liu CH,Marianna DA,Gaca E,et al.Smads 2 and 3 are differentially activated by transforming growth factor-β (TGF-β) in quiescent and activated hepatic stellate cells[J].J Biol Chem,2003;278(13):11721-11728.
  • 3Kondou H,Mushiake S,Etani Y,et al.A blocking peptide for transforming growth factor-beta 1 activation prevents hepatic fibrosis in vivo[J].J Hepatol,2003;39(5):742-748.
  • 4Dooley S,Hamzavi J,Breitkopf K,et al.Smad 7 prevents activation of hepatic stellate cells and liver fibrosis in rats[J].Gastroenterology,2003;125(1):178-191.
  • 5Caestecker M P, Piek E, Roberts A. Role of growth factor-βsignaling in cancer. J Natl Cancer Inst, 2000,92: 1388-1402.
  • 6Wilentz R E, Su G H, Dai J L, et al. Immunohistochemical labeling for DPC4 mirrors genetic status in pancreatic adenocarcinomas: a new marker of DPC4 inactivation. Am J Pathol, 2000, 156: 37-43.
  • 7Maliekal T T, Antony M L, Nair A, et al. Loss of expression, and mutations of Smad 2 and Smad 4 in human cervical cancer. Oncogene,2003, 22: 4889- 4897.
  • 8Piestrzeniewicz-Ulanska D, Brys M, Semczuk A, et al.Expression and intracellular localization of Smad proteins in human endometrial cancer. Oncol Rep, 2003,10: 1539-1544.
  • 9Nicolas F J, Hill C S. Attenuation of the TGF-betaSmad signaling pathway in pancreatic tumor cells confers resistance to TGF-beta-induced growth arrest. Oncogene, 2003, 22: 3698-3711.
  • 10van der Poel H G, Hanrahan C, Zhong H, et al. Rapamycin induces Smad activity in prostate cancer cell lines. Urol Res, 2003, 30: 380-386.

共引文献48

同被引文献5

引证文献1

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