Preliminary study of the role of canonical Wnt signalling pathway in non-Hodgkin's lymphoma cell lines
10.3781/j.issn.1000-7431.2013.02.007
- Author:
Qi QU
1
Author Information
1. Department of Hematology
- Publication Type:Journal Article
- Keywords:
β-catenin;
Glycogen synthase kinase 3;
Lymphoma;
Non-Hodgkin;
Wnt signaling pathway
- From:
Tumor
2013;33(2):144-149
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To determine whether the canonical Wnt signalling pathway is abnormally activated in NHL (non-Hodgkin's lymphoma), and to explore its association with pathogenesis of NHL. Methods: The expression levels of β-catenin, GSK-3β (glycogen synthase kinase-3β) and its inactive form p-GSK-3β (Ser9) (phosphorylation of GSK-3β at Ser9 residue) in NHL cell lines including SUDHL-4, Raji and Namalwa were detected by Western blotting, and the normal human lymphocytes were served as the controls. The mRNA levels of CTNNB 1 gene (encoding β-catenin), canonical Wnt signaling pathwayrelevant gene LRP 5 (low-density lipoprotein receptor-related protein 5) and target gene c -Myc were detected by real-time fluorogenic quantitative PCR. Results: The expressions of total cellular proteins and β-catenin protein in cell nuclei were significantly up-regulated in three NHL cell lines as compared with in those normal human lymphocytes. The elevated expression levels of p-GSK-3β (Ser9) were observed in lymphoma cell lines, but the expression level of GSK-3β was not significantly different between the lymphoma cell lines and the normal human lymphocytes. The mRNA expression levels of CTNNB1, LRP5 and c-Myc were significantly higher in lymphoma cell lines than those in the normal human lymphocytes. Conclusion: Given the important role of β-catenin as an activation marker in canonical Wnt signaling pathway, the evidence of up-regulated expression of β-catenin and the changes of other relevant molecules in canonical Wnt signaling pathway suggests that the constitutional activation of canonical Wnt signaling pathway may contribute to the pathogenesis of NHL. Copyright © 2013 by TUMOR.
