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Figure 5 | Journal of Hematology & Oncology

Figure 5

From: Galectin-3 mediates bone marrow microenvironment-induced drug resistance in acute leukemia cells via Wnt/β-catenin signaling pathway

Figure 5

Gal-3 up-regulation promotes phosphorylation of Akt and GSK-3β, thereby supporting β-catenin stabilization. (A) The protein level of phosphorylated Akt (Pho-Akt), total Akt (T-Akt), phosphorylated GSK-3β (Pho-GSK-3β), and total GSK-3β (T-GSK-3β) expressed in ALCs cultured alone or with hBM-MSCs. Increased gal-3 in hBM-MSC-conditioned ALCs was associated with increased phosphorylation of Akt and GSK-3β while the total protein expression remained unchanged. (B) The protein level of Pho-GSK-3β and T-GSK-3β in gal-3-silenced Kasumi-1 and Reh cells, cultured alone or with hBM-MSCs. (C) The time-dependent changes of Pho-GSK-3β and β-catenin in hBM-MSC-conditioned Kasumi-1 and Reh cells. The densitometry data was measured using Quantity One software, calculated as Pho-GSK-3β/T-GSK-3β compared with the level at 0 h. (D) Expression of β-catenin after treatment with LY294002 (25 μM) in hBM-MSC-conditioned Kasumi-1 and Reh cells. (E) The mRNA levels of gal-3 expressed in AL patients (P < 0.01). We enrolled 40 patients in all, including 13 primary AML, 13 refractory/relapsed AML and 7 primary ALL, 7 refractory/relapsed ALL. (F) Western blot analysis of gal-3/β-catenin axis in AL patients-derived malignant cells cultured with or without hBM-MSCs. Data are from one AML and one ALL patients, representative of the patients examined.

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