Skip to main content
. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Cancer Res. 2015 Dec 16;76(3):675–685. doi: 10.1158/0008-5472.CAN-15-1141

Figure 5.

Figure 5

AKT depletion decreased pS21-EZH2, phospho-STAT3, and methyl K levels strongly in cell lines expressing KRASG12D mutants. A and B, EZH2, pS21-EZH2, STAT3, phospho-STAT3, and methyl K level expression in NSCLC cell lines and HBEC cell lines. KRASWT and KRAS mutants were treated with different doses of the AKTi MK2206 (0, 25, and 50 nM). C, EZH2, pS21-EZH2, STAT3, phospho-STAT3, and methyl K level expression in NSCLC cell lines expressing KRASG12C and KRASG12D mutants upon knockdown of AKT1, AKT2, and AKT3 expression by treatment with siAKT. D, EZH2, pS21-EZH2, STAT3, phospho-STAT3, and methyl K level expression in NSCLC cell lines expressing KRASG12C and KRASG12D mutants upon knockdown of EZH2. E, Proposed model showing EZH2 as a downstream effector of KRAS signaling in malignant cell KRAS mutants.