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. Author manuscript; available in PMC: 2016 Aug 10.
Published in final edited form as: Cancer Cell. 2015 Aug 10;28(2):240–252. doi: 10.1016/j.ccell.2015.07.005

Figure 6. Mechanistic model of SRC hyper-activation by MCB-613.

Figure 6

By directly binding to SRCs, MCB-613 increases the interaction between SRCs and other coactivators such as CBP and CARM1. Meanwhile, the resultant elevated ROS activates Abl kinase which phosphorylates and further hyper-activates SRCs. The deregulation of cellular functions and homeostasis downstream of SRCs hyper-activation strongly induces ER stress and UPR, producing more ROS and forming a positive feedback loop. The resultant excessive ER and oxidative stress overwhelms cancer cells, leading to vacuolization and cell death.