High expression and nuclear localization of β-catenin in diffuse large B-cell lymphoma

被引:32
作者
Ge, Xueling [1 ]
Lv, Xiao [1 ]
Feng, Lili [1 ]
Liu, Xiaoqian [2 ]
Wang, Xin [1 ]
机构
[1] Shandong Univ, Prov Hosp, Dept Hematol, Jinan 250021, Shandong, Peoples R China
[2] Qingdao Univ, Coll Med, Affiliated Hosp, Dept Hematol,Yantai Yuhuangding Hosp, Yantai 264000, Shandong, Peoples R China
关键词
diffuse large B-cell lymphoma; beta-catenin; nuclear localization; signaling pathway; RETRACTED ARTICLE. SEE; WNT CANONICAL PATHWAY; SIGNALING PATHWAYS; SURVIVAL; LEUKEMIA; KINASE; OVEREXPRESSION; ACTIVATION; BINDING; CANCER;
D O I
10.3892/mmr.2012.835
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The Wnt/beta-catenin signaling pathway plays diverse roles in embryonic development and maintenance of organs and tissues in adults as well as in the pathogenesis of a range of diseases, including many types of carcinomas. beta-catenin, the principal downstream effector of the Wnt/beta-catenin pathway, migrates to the nucleus and mediates the activation of the Wnt/beta-catenin pathway. The aim of the present study was to investigate the expression and localization of beta-catenin in diffuse large B-cell lymphoma (DLBCL) tissues and to illuminate the role of beta-catenin in the pathogenesis of DLBCL. The mRNA expression levels of beta-catenin were determined by quantitative polymerase chain reaction (PCR), while beta-catenin protein levels were detected by western blot analysis and immunohistochemical staining. DLBCL showed a higher expression of beta-catenin in contrast to reactive hyperplasia of lymph node tissues at both the mRNA and protein levels (P<0.001). Immunohistochemical analysis indicated nuclear localization of beta-caten in in 14(46.67%) DLBCL cases, whereas no inflammatory lymph node tissue showed nuclear accentuation of beta-catenin. The overexpression and nuclear accentuation of beta-catenin were strongly correlated to the clinical staging of patients with DLBCL (P<0.05). These results suggest that the Wnt/beta-catenin pathway is partly activated in DLBCL and may contribute to its pathogenesis.
引用
收藏
页码:1433 / 1437
页数:5
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