Fig. 6

B56γ3 reduces the sensitivity of CRC cells to 5-FU. A HCT116 and B SW480 cells with control vector (shLuc) or stable knockdown of B56γ3 (shB56γ3) were treated with 0, 25, 50, 75, and 100 μM 5-FU for 72 h, and cell viability was measured using the Presto Blue viability assay according to the manufacturer’s protocol. C HCT116 cells with vector only (pMSCV) or stably overexpressing B56γ3 (4HAB56γ3) were treated with 5-FU, and cell viability was measured as described previously. The IC50 of 5-FU was analyzed using GraphPad Prism version 5 for Windows. D HCT116 cells with vector (pMSCV) or stable overexpression of B56γ3 (4HAB56γ3) were treated with 5-FU (50 μM) or 5-FU (50 μM) and MK-2206 (50 μM) for 24 h, and cell viability was measured as described previously. E Lysates of HCT116 cells with vector only (pMSCV) or B56γ3 overexpression (4HAB56γ3) treated with 5-FU or 5-FU and MK2206 for 24 h were analyzed by SDS-PAGE and Western blotting with the indicated antibodies. F The PP2A-B56γ3 holoenzyme upregulates AKT activation to promote EMT and the potential of drug resistance by downregulating p70S6K activity and attenuating the p70S6K-mediated negative feedback loop regulation of growth factor-stimulated PI3K/AKT activation. The dashed line indicates that the PP2A-B56γ3 holoenzyme indirectly activates AKT activity