Fig. 2.

Model for the regulation of apoptosis by Gal-3. Anticancer drugs can induce DNA damage, which causes Gal-3 phosphorylated by Casein Kinase 1 (CK1) translocate from the nuclear to cytoplasm. Gal-3 upregulates the ERK pathway and induces Bad phosphorylation, leading to mitochondrial stabilization. Akt activated by Gal-3 inhibits apoptosis by blocking transformation of Bid into tBid, which is essential for cytochrome c release from the mitochondrial intermembrane space. After treatment of proapoptotic agents, Gal-3 in cytoplasm decreases Bad expression and attenuates the depolarization of the mitochondrial membrane. Consequently, the stabilization of the mitochondrial membrane prevents cytochrome c release and subsequent caspase activation, resulting in suppression of apoptosis and resistance to chemotherapeutic agents