期刊文献+

Peroxiredoxin Ⅱ在卵巢上皮性肿瘤中的表达及其临床意义 被引量:2

Expression of Peroxiredoxin Ⅱ in ovarian cancer:correlation with clinicopathological features
下载PDF
导出
摘要 目的探讨Peroxiredoxin Ⅱ在卵巢上皮性肿瘤组织中的表达及临床意义。方法用蛋白免疫印迹(westernblot)的方法检测71例新鲜卵巢组织及卵巢上皮肿瘤组织的Peroxiredoxin Ⅱ的表达情况,其中正常卵巢组织16例,良性卵巢肿瘤16例,卵巢癌39例。结果Peroxiredoxin Ⅱ在正常卵巢组织表达为(1.00±0.44),在良性卵巢上皮性肿瘤组织中表达为(0.83±0.50),在卵巢癌组织中表达为(0.60±0.23),卵巢癌与正常卵巢组织的表达差异有显著性(P<0.01);良性卵巢上皮性肿瘤组织与正常卵巢组织、癌组织比较差异均无统计学意义;且Peroxiredoxin Ⅱ在卵巢癌组织表达降低与其临床分期、病理类型、细胞分化及绝经等参数无关。结论Peroxiredoxin Ⅱ可能在卵巢上皮癌的发生中起抑制因子作用,而在其发展中无明显作用。 [Objective] To investigate the significance of Peroxiredoxin Ⅱ expression with carcinogenesis and progression in ovarian cancer. [Method] Western blot was used to investigate the expression of Peroxiredoxin Ⅱ in 16 cases of nomal ovarian tissue, 16 cases of benign ovarian tumor, and 39 cases of ovarian cancer. [Result] Expression of Peroxiredoxin Ⅱ in nomal ovarian tissue (1.00±0.44) and benign ovarian tumor(0.83±0.50) was higher than that in ovarian cancer (0.63±0.23). There was a significant difference in the expression of Peroxiredoxin Ⅱ between nomal ovarian tissue (1.00±0.44) and ovarian cancer 0.63±0.23) (P 〈0.05). There was no relationship between the expression of Peroxiredoxin Ⅱ and clinicopathological parameters, including cilical stage, tumor cell differentiation degree, histopathologic classification, and menopause. [ Conclusion] Peroxiredoxin Ⅱ highly expressed in normal ovarian tissue and benign ovarian tumor while low expressed in ovarian cancer. Our findings suggest that high expression of Peroxiredoxin Ⅱ may play an important role as a suppressor factor in carcinogenesis in ovarian tumor not in tumor progression in ovarian cancer.
出处 《中国现代医学杂志》 CAS CSCD 北大核心 2007年第22期2773-2776,共4页 China Journal of Modern Medicine
关键词 PEROXIREDOXIN 良性卵巢上皮肿瘤 卵巢上皮性癌 Peroxiredoxin benign ovarian tumor epithelial ovarian carcinoma.
  • 相关文献

参考文献1

共引文献13

同被引文献43

  • 1章波,向渝梅,白云.抗氧化蛋白Peroxiredoxin家族研究进展[J].生理科学进展,2004,35(4):352-355. 被引量:41
  • 2杨柳,米粲,霍艳英.Peroxiredoxin在H_2O_2介导的信号通路中的作用[J].国际病理科学与临床杂志,2006,26(5):417-419. 被引量:7
  • 3Ziecha D, Franco R, Pappa A et al. Reactive oxygen species (ROS)-induced genetic and epigenetic alterations in human carcinogenesis[ J]. Murat Res, 2011,711 ( 1-2 ) : 167-173.
  • 4Thannickal V J,Fanburg B. Reactive oxygen species in signaling [J]. Am J Physiol Lung Cell Mol Physiul,2000, 297(6) :LI005- 1028.
  • 5Phalen T J, Weirather K, Deming P B, et al. Oxidation state governs structural transitions in peroxiredoxin I1 that correlate with cell cycle arrest and recovery [ J ]. J Cell Biol, 2006, 175 ( 5 ) : 779-789.
  • 6Yuan Z, Schellekens H, Warner L, et al. Reactive nitrogen species block cell cycle re-entry through sustained production of hydrogen peroxide [ J ]. Am J Respir Cell Mol Biol, 2003, 28 (6) :705-712.
  • 7Butch P M, Ynan Z, Loonen A, et al. An extraeellular signal regulated kinase l-and 2-dependent program of chromatin trafficking of c-Fos and Fra-1 is required for cyclin DI expressionduring cell cycle reentry [ J ]. Mol Cell Biol, 2004, 24 (11): 4696-4709.
  • 8Singh M, Sharrna H, Singh N. Hydrogen peroxide induces apoptosis in HeLa cells through Mitoehondrial pathway [ J ]. Mitoehondrion, 2007, 7(6) :36%373.
  • 9Rhee S G, Kang S W, Jeong W, et aL Intracellular messenger function of hydrogen peroxide and its regulation by peroxiredoxins [J]. Curr Opin Cell Biol, 2005, 17(2) :183-189.
  • 10Ruffels J, Griffin M, Dickenson J M. Activation of ERK1/2 ,JNK and PKB by hydrogen peroxide in human SH-SY5Y neuroblastoma cells:role of ERK1/2 in H2 02 -induced cell death [ J ]. Eur J Pharmacol, 2004, 483 ( 2-3 ) : 163-173.

引证文献2

二级引证文献4

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