Figure 1. Coactivation of the MAPK and PI3K/AKT pathways in RAS-mutated EGFR-positive cancer cells.

(A) A431 cells were retrovirally transduced to stably express the oncogenic RAS mutant HRAS^G12V. Constitutive and ligand-induced (EGF 10 ng/ml) phosphorylation of PI3K/AKT and MAPK signal transducers AKT and ERK1/2 in A431-HRAS^G12V cells or controls. ACTIN serve as control for equal loading. (B) A431-RAS wild type cells were retrovirally transduced to stably express a ΔRAF-1/ER^Tam- or a myristoylated-AKT/ER^Tam (myr-AKT/ER^Tam) construct. Phosphorylation of RAF-1 was strongly induced in A431-ΔRAF-1/ER^Tam cells and phosphorylation of myr-AKT/ER^Tam was strongly induced in A431-myr-AKT/ER^Tam cells by the addition of 4-hydroxytamoxifen (4-OHT).