Fig. 6. Schematic representation of the mechanisms underlying apoptosis induced by vorinostat in combination with QC.

The treatment with vorinostat in combination with QC induced an increase in the level of intracellular ROS, further promoting mitochondrial dysfunction and the accumulation of K63-linked ubiquitination of the mitochondria, which indicates mitophagy. QC blocked autophagy flow through lysosomal dysfunction, resulting in the accumulation of mito-aggresomes and eventually inducing T-ALL cell death