Figure 7.

Schematic representation of SNA-mediated induction of apoptosis in OAW-42 cells. Hyper-sialylation associated with OC drives SNA binding to these cells leading to the activation of AKT and ERK1/2 pathways. Meanwhile in response to SNA administration, mitochondrial membrane permeabilization occurs in association with cytochrome-c release into the cytosol and ROS generation leading to mitochondrial dysfunction. The resulting shift in the cellular bioenergetics promotes cell cycle arrest finally culminating into apoptosis via caspase activation