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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: The B56γ3-containing protein phosphatase 2A attenuates p70S6K-mediated negative feedback loop to enhance AKT-facilitated epithelial-mesenchymal transition in colorectal cancer

Fig. 2

B56γ3 upregulates AKT phosphorylation in response to growth factor stimulation. A, B Lysates of HeLa cells with shLuc or stable knockdown of B56γ3(shB56γ3) stimulated by EGF (50 ng/ml) or insulin (100 nM), respectively, at the indicated time points, C Lysates of SW480 with shLuc or stable knockdown of B56γ3 (shB56γ3) stimulated by IGF-1 (50 ng/ml) at the indicated time points, and D Lysates of HCT116 cells with shLuc or stable knockdown of B56γ3(shB56γ3) stimulated by EGF (20 ng/ml) at the indicated time points were analyzed by SDS-PAGE and Western blotting with antibodies as indicated. The mean relative expression levels of p-Akt at Thr308 (T308) and Ser473 (S473) of three independent experiments with similar results were quantitated as described earlier. Graphs show comparisons of the peak levels (A, B) of phospho-AKT (Thr308 and Ser473) or levels of phospho-Akt (Thr308 and Ser473) at different time points (C, D) stimulated by growth factors between control shLuc and stable knockdown (shB56γ3). The differences were assessed for statistical significance by Student’s t test with p-values (*(< 0.05), **(< 0.01), ***(< 0.001)). (n = 3)

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