p62/SQSTM1 signaling nexus and orchestration of ERK and mTOR pathways are crucial for Bacoside A- induced autophagy-mediated apoptosis in chronic myelogenous leukemia.

This study investigates the anticancer potential of Bacoside A (BCA), a compound derived from the herb Bacopa monnieri, against chronic myelogenous leukemia (CML) cells. BCA was found to selectively induce cytotoxicity in CML cells while sparing normal cells. Mechanistically, BCA triggered a biphasic response - first inducing autophagy, followed by caspase-dependent apoptosis. The p62/SQSTM1 protein played a key role in this process, acting as a positive regulator of autophagy and a bridge between autophagy and apoptosis. BCA also modulated the ERK and mTOR signaling pathways, which were crucial for the observed effects. These findings uncover a novel mechanism of action for BCA in CML, highlighting its potential as a therapeutic agent. Limitations include the need for further in vivo validation and exploration of the