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Proposed model in which gal-3 mediates Wnt/β-catenin signaling in the BMM-induced drug resistance of AL. hBM-MSCs induce gal-3 expression in ALCs. Gal-3 mediates Akt phosphorylation, which promotes phosphorylation of GSK-3β and thus decreases its activity. Inactivation of GSK-3β leads to a reduction in β-catenin degradation. Stabilized β-catenin translocates to the nucleus and activates transcription of its specific target genes, which ultimately leads to drug resistance in ALCs.
