Figure 7. Schema of the predicted mechanisms implicated in glioma cells response to TRAIL and miR-125b. Overexpression of miR-125b suppressed the expression of TAZ, and thus promoted the TRAIL-dependent collapse of outer mitochondrial membrane potential and permeability. As the results, combination with miR-125b and TRAIL induced release of cytochrome c into the cytoplasm from the damaged mitochondria. In the presence of cytochrome c, caspase-9 and its downstream caspase-3 was cleaved. Finally, the caspases-dependent apoptosis occurs.