Specific Inhibition of β-Catenin in Jeko-1 Mantle Cell Lymphoma Cell Line Decreases Proliferation and Induces Apoptosis

Background: The canonical Wnt signaling pathway has been considered as a potent oncogenic signaling in the initiation and progression of hematological malignancies. As a key regulator of the Wnt signaling pathway, the role of beta-catenin in mantle cell lymphoma (MCL) pathogenesis and progression was investigated in this study. Material/Methods: A total of 30 MCL samples were collected from patients and were examined for the expression of beta-catenin and p-GSK3 beta using immunohistochemical (IHC) staining. Further in vitro studies employed MTT and Western blot assays detecting proliferation and apoptosis-related proteins in MCL cell line Jeko-1, which were transfected with beta-catenin shRNA or specific inhibitor XAV939. Results: Expression of beta-catenin and phosphorylated glycogen synthase kinase-3 beta (p-GSK3 beta) in MCL was significantly higher than those in controlled samples. In vitro studies indicated that beta-catenin knockdown significantly inhibited cell proliferation and induced apoptosis in Jeko-1 cells. Furthermore, XAV939 induced apoptosis and growth arrest in Jeko-1 cells. Both inhibitory agents increased Bax and caspase 3 proteins, and decreased Bcl-2, c-Myc, and Cyclin D1 proteins. Conclusions: The specific inhibition of beta-catenin induces apoptosis and growth arrest, making it a potential therapeutic target against MCL.