Skip to main content
. Author manuscript; available in PMC: 2014 May 19.
Published in final edited form as: J Cancer Ther. 2014 Jan;5(1):124–131. doi: 10.4236/jct.2014.51015

Figure 3.

Figure 3

SYK as a Master Regulator of Apoptosis. Several chemotherapy drugs as well as radiation therapy exert their anti-cancer activity by inducing oxidative stress (OS). OS exposure of BPL cells triggers the activation of PLK1, which then activates SYK. Activation of SYK results in stimulation of the anti-apoptotic NFkB, STAT3, and PI3-K/AKT pathways and thus contributes to the frequently observed resistant phenotype of BPL cells. Inhibition of SYK with the small molecule inhibitor C61 directly inactivates SYK and causes apoptosis.