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. 2017 Apr 26;8(28):45898–45917. doi: 10.18632/oncotarget.17438

Figure 7. Combined pharmacologic targeting of MAPK and PI3K/AKT signaling resensitizes EGFR positive cells to anti-EGFR therapies.

Figure 7

(A) Proliferation of Difi-HRASG12V cells grown in the presence of cetuximab (100 ng/ml), the MEK inhibitor U0126 (1 μM) or in combination. Mean values (± SD) of three independent MTT assays. (B) Immunoblot analysis of HCT116 which harbors an endogenous KRAS exon 2 and an additional PIK3CA exon 20 mutation treated with cetuximab (20 μg/ml), the PI3K inhibitor Ly294002 (10 μM), the MEK inhibitor U0126 (1 μM) and in combination. Inhibition of constitutive phosphorylation of MAPK and PI3K/AKT signal transducers ERK1/2 and p70S6 by the pharmacological inhibitors Ly294002 and U0126, respectively. (C) Proliferation of HCT116 cells grown in the presence of cetuximab (20 μg/ml), the PI3K inhibitor Ly294002 (10 μM), the MEK inhibitor U0126 (1 μM) and in combination. Mean values (± SD) of three independent MTT assays. (D) Fraction of apoptotic HCT116 cells with subgenomic DNA content (sub-G1) following treatment with cetuximab (20 μg/ml], Ly294002 (15 μM), U0126 (1 μM) and in combination (mean ± SD of three independent experiments).