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. 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 4.

Figure 4

EZH2 expression is regulated by MEK-ERK and PI3K/AKT signaling pathways in colon and pancreatic tumor KRAS mutants. A, top panel, EZH2, MAPK P44/42, and phospho-MAPK P44/42 expression in colon and pancreatic cell lines. KRASWT and KRAS mutants were treated with different doses of the MEK1i AZD6244 (0, 0.5, and 1.0 μM). A, bottom, EZH2, AKT, and phospho-AKT expression in colon and pancreatic cell lines. KRASWT and KRAS mutants were treated with different doses of the AKTi MK2206 (0, 25, and 50 nM). B, top, EZH2 inhibition with DZNep in combination with MEK1i. (Data are graphed as the mean percent increase ± percent standard deviation). Treatment with DZNep caused a 16-fold (P < 0.03) decrease in the AZD6244 IC50 in MIA PaCa2 cells. B, bottom, EZH2 inhibition with DZNep in combination with AKTi. (Data are graphed as the mean percent increase ± percent standard deviation). Treatment with DZNep caused a decrease in MK2206 IC50, 10.6-fold (P < 0.03) in cells expressing KRASG12C, a 6.4-fold (P < 0.05) in cells expressing KRASG12D and a 6.8-fold (P < 0.05) in cells expressing KRASG12D.