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作 者:吴晓慧[1] 王顺祥[1] 杨永江[1] 李建坤[1] 彭利[1] 唐瑞峰[1] 王士杰[2]
机构地区:[1]河北医科大学第四医院肝胆外科,石家庄050011 [2]河北医科大学第四医院肿瘤研究所,石家庄050011
出 处:《肿瘤》2008年第10期869-872,共4页Tumor
摘 要:目的:探讨Raf激酶抑制蛋白(Raf kinase inhibitor protein,RKIP)和磷酸化细胞外信号调节激酶(phos-extracellular signal regulated kinase,P-ERK)在肝细胞癌(hepatocellular carcinoma,HCC)中的表达及其临床意义。方法:应用免疫组织化学方法检测RKIP和P-ERK在HCC、癌旁及正常肝组织中的表达,并分析其与HCC临床病理学特征的关系。结果:HCC组织中RKIP的表达低于癌旁及正常肝组织,而P-ERK的表达高于癌旁及正常肝组织,差异有统计学意义;HCC组织中RKIP与P-ERK的表达呈显著负相关(r=-0.227,P=0.039);RKIP在HCC组织中的表达与有无肝内或淋巴结转移及肿瘤分化程度相关(P<0.05);P-ERK在HCC组织中的表达与肿瘤分化程度、有无癌栓及有无肝内或淋巴转移相关(P<0.05)。结论:RKIP表达的减少或缺失与HCC的发生、发展密切相关,RKIP表达的减少或缺失可能通过上调P-ERK的表达促进HCC的侵袭和转移。Objective:To investigate the expression and clinical significance of Raf kinase inhibitor protein (RKIP) and phos-phorylated-extracellular signal regulated kinase (P-ERK) in hepatocellular carcinoma (HCC) and their correlations with the invasion and metastasis of HCC. nethods:Immunohistochemistry was used to detect the expressions of RKIP and P-ERK in HCC tissues, paracancerous tissues, and normal liver tissues. Statistical analysis was used to determine the relationship between their expressions and clinicopathological parameters. Results: Statistical analysis revealed that RKIP-positive staining rate was lower in tumor tissues than that in tumor-surrounding tissues and in normal liver tissues. But P-ERK-positive staining rate was significantly higher in tumor tissues than that in tumor-surrounding tissues and normal liver tissues. The difference was significant. RKIP expression had negative correlation with P-ERK expression (r = - 0. 227, P = 0.039) ; RKIP expression in HCC was associated with intrahepatic or lymphatic metastasis and tumor differentiation ( P 〈 0.05 ). P-ERK expression in HCC was related with tumor differentiation, tumor thrombosis, and intrahepatic or lymphatic metastasis ( P 〈 0.05 ). Conclusions: These findings indicate that down-regulation or loss of RKIP expression is closely related with HCC development and progression. The down-regulation or loss of RKIP expression stimulates migration and metastasis of HCC by up-regulating P-ERK expression.
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