Figure 3: Ectopic R-RAS2G23V and endogenous R-RAS regulate the PI3Kα/AKT route in MDA-MB-231-Luc cells. | Nature Communications

Figure 3: Ectopic R-RAS2G23V and endogenous R-RAS regulate the PI3Kα/AKT route in MDA-MB-231-Luc cells.

From: Contribution of the R-Ras2 GTP-binding protein to primary breast tumorigenesis and late-stage metastatic disease

Figure 3

(a) Phosphorylation and expression status of ERK and AKT proteins (left) in indicated MDA-MB-231-Luc cells (top) under exponentially growing (+ Serum) and serum-free (– Serum) conditions. p, phosphorylated. (b) Akt phosphorylation in indicated serum-starved MDA-MB-231-Luc cells (bottom) treated with PI3K family (LY294002, 20 μM), PI3Kα (PIK-75, 1 μM), PI3Kβ (TGX-221, 0.5 μM), PI3Kδ (IC-87114, 5 μM) and PI3Kγ (AS-252424, 0.5 μM) inhibitors (top). (c) Phosphorylation kinetics of AKT and FOXO1/3a in indicated, IGF1-stimulated MDA-MB-231-Luc cells. (d) Quantitation of phosphorylation kinetics of indicated proteins in above experiments (n=3). *P≤0.05; **P≤0.01 relative to values obtained in non-stimulated cells (which were given an arbitrary value of 1); t-test. (e) Phosphorylation kinetics of AKT and FOXO1/3a in indicated, EGF-stimulated MDA-MB-231-Luc cells. (f) Quantitation of phosphorylation kinetics of indicated proteins in above experiments (n=3). *P≤0.05; **P≤0.01 relative to values obtained in non-stimulated cells (which were given an arbitrary value of 1); t-test. In panels d and f, experimental values are given as mean±s.e.m.

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