期刊文献+

Stat3磷酸化与c-fos和c-jun蛋白表达在肝细胞癌发生中的作用 被引量:7

Effects of Stat3 phosphorylation and expression of c-fos and c-jun proteins on hepatocarcinogenesis
下载PDF
导出
摘要 利用SP免疫组织化学技术检测 5 5例肝细胞癌 (HCC)及其癌旁组织中p Stat3(Tyr70 5 ) ,c fos和c jun蛋白的表达。结果显示 :HCC中p Stat3,c fos和c jun蛋白阳性率和阳性强度均高于癌旁组织 (P <0 .0 1) ,且p Stat3与c fos和c jun蛋白表达强度均呈明显正相关 ,而在癌旁组织中p Stat3仅与c jun蛋白表达相关 ,提示Stat3蛋白的磷酸化可能是HCC发生的早期事件 ,并通过激活c jun和c fos基因使肝细胞恶性转化 ;癌旁肝组织中 ,p Stat3,c jun或c fos呈阳性表达的肝细胞可能是一种具有恶性潜能的癌前细胞群。 Expression of phosphorylated Stat3 (p Stat3), c fos and c jun proteins was detected by immunohistochemical technique in 55 hepatocellular carcinomas (HCC) and their surrounding liver tissues. The results showed that the positive rates and signal intensity of p Stat3, c fos and c jun protein in HCCs were significantly higher than those in pericarcinomatous tissues. The expressive intensity of c fos and c jun proteins was positively related to p Stat3 expression in HCCs, whereas the positive correlation of expressive intensity was only observed between c jun protein and p Stat3 in pericarcinomatous tissues. The data suggest that the phosphorylation of Stat3 may be an early event in hepatocarcinogenesis; the overexpression of p Stat3 protein, which activates c fos and c jun genes, may contribute to malignant transformation of hepatocytes; hepatocytes which expressed p Stat3, c fos or c jun proteins may be potentially malignant pre cancer cells in pericarcinomatous liver tissues. [
出处 《湖南医科大学学报》 CSCD 北大核心 2001年第1期17-19,共3页 Bulletin of Hunan Medical University
关键词 信号传导 转录激活因子3 C-FOS蛋白 C-JUN蛋白 肝细胞癌 liver neoplasm signal transducer and activator of transcription 3 * signal transduction oncogen
  • 相关文献

参考文献3

  • 1Chung J,Mol Cell Biol,1997年,17卷,6508页
  • 2Wen Z,Cell,1995年,82卷,241页
  • 3Fromowitz F B,Hum Pathology,1987年,18卷,1268页

同被引文献162

  • 1De Yun Feng,Hui Zheng,Yi Tan,Rui Xue Cheng Department of Pathology, Hunan Medical University, Changsha 410078, Hunan Province, China New England Biolab, MA, USA.Effect of phosphorylation of MAPK and Stat3 and expression of c-fos and c-jun proteins on hepatocarcinogenesis and their clinical significance[J].World Journal of Gastroenterology,2001,7(1):33-36. 被引量:75
  • 2Darnell J E Jr. STATs and gene regulation[J]. Science, 1997,277 (5332):1630-1635.
  • 3Schindler G, Damell J E Jr. Transcriptional responses to polypeptide ligands: the JAK-STAT pathway [J]. Annual Review of Biochemistry, 1995,64:621-651.
  • 4Tweardy D J, Jing N. Enhancing or eliminating signals for cell survival to treat disease[J]. Trans Am Clin Climatol Assoc, 2006,117: 33-52.
  • 5Fu A K, Fu W Y, Ng A K. Cyclin-dependent kinase 5 phospho-rylates signal transducer and activator of transcription 3 and regulates its transcriptional activity[J]. Prec Natl Acad Sci USA, 2004, 101(17):6728-6733.
  • 6Lira C P, Cao X. Serine phosphorylation and negative regulation of Stat3 by JNK[J]. J Biol Chem, 1999,274(43):31055-31061.
  • 7Jain N, Zhang T, Fong S L, et al. Repression of Stat3 activity by activation of mitogen-activated protein kinase(MAPK)[J]. Oncogene, 1998,17(24):3157-3167.
  • 8Abe K, Hirai M, Mizuno K, et al. The YXXQ motif in gp 130 is crucial for STAT3 phosphorylation at Ser727 through an HT-sensitive kinase pathway[J]. Oncogene, 2001,20(27):3464-3474.
  • 9LO R K, Cheung H, Wang Y H. Constitutively active Galpha16 stimulates STAT3 via a c-Src/JAK- and ERK-dependent mechanism[J]. J Biol Chem, 2003,278(52):52154-52165.
  • 10Herrmann A, Vogt M, Monnigmann M, et al. Nucleocytoplasmie shuttling of persistently activated STAT3[J]. J Cell Sci, 2007,120(Pt 18):3249-3261.

引证文献7

二级引证文献96

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