首页> 中文期刊>实用妇产科杂志 >卵巢上皮性癌中Raf激酶抑制蛋白、核因子κBp65蛋白的表达及相关性研究

卵巢上皮性癌中Raf激酶抑制蛋白、核因子κBp65蛋白的表达及相关性研究

     

摘要

目的:研究卵巢上皮性癌组织中Raf激酶抑制蛋白(RKIP),核因子KBp65蛋白(NF-κBp65)的表达,探讨两者在卵巢上皮性癌侵袭转移中的作用和机制,分析RKIP表达水平改变对卵巢上皮性癌侵袭能力和NF-κB信号通路活性的影响.方法:应用免疫组织化学染色方法检测76例卵巢上皮性癌组织、35例良性卵巢上皮性肿瘤组织、22例正常卵巢组织中RKIP和NF-κBp65蛋白的表达,并分析不同卵巢组织临床及病理因素之间的关系.结果:卵巢上皮性癌组织中RKIP的表达低于良性卵巢上皮性肿瘤组织及正常卵巢组织,而NF-κBp65的表达高于良性卵巢上皮性肿瘤组织及正常卵巢组织,差异有高度统计学意义(P<0.01);RKIP和NF-κBp65在卵巢上皮性癌中的表达均与肿瘤分化程度、临床分期及有无淋巴结转移有关(P<0.05);卵巢上皮性癌组织中RKIP与NF-κBp65的表达呈负相关(r=-0.582,P<0.01).结论:RKIP表达的减少或缺失与卵巢上皮性癌的发生、发展密切相关,可能通过上调NF-κBp65的表达促进卵巢上皮性癌的侵袭和转移,其机制可能与活化NF-κB信号通路有关.%Objective:To investigate the expression of Raf kinase inhibitor protein (RKIP) and nuclear factor kappa Bp65(NF-κBp65) and its role and mechanism in the invasion and metastasis of epithelial ovarian cancer. To analyze the effects of RKIP expression on the epithelial ovarian cancer invasion, and the activity of NF-κB signaling pathway. Methods: Immunohistochemistry was used to detect the expression of RKIP and NF-κBp65 in 76 cases of epithelial ovarian cancer,35 cases of epithelial ovarian benign neoplasms,and 22 cases of normal ovary. The relationship between clinic and pathological factors in different ovarian tissues were analyzed. Results:The expression of RKIP was lower in epithelial ovarian cancer than that in epithelial ovarian benign neoplasms and normal ovary, while the expression of NF-κBp65 in epithelial ovarian cancer was higher than that in epithelial ovarian benign neoplasms and normal ovary. There was significant difference between them( P<0. 01 ).The expression of RKIP and NF-κBp65 in the epithelial ovarian cancer were associate with tumor differentiation, clinical staging, lymphnode metastasis( P<0. 05). RKIP expression was negatively correlated with NF-κBp65 ( r= -0. 582 ,P<0. 01 ). Conclusions:Down-regulation or loss of RKIP expression is closely related with the development and progression of epithelial ovarian cancer, which facilitates the invasion and metastasis of epithelial ovarian cancer by up-regulating NF-κBp65 expression. The mechanism maybe activate the NF-κB signaling pathway.

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