Skip to main content
Fig. 5 | Breast Cancer Research

Fig. 5

From: Activation of IGF1R/p110β/AKT/mTOR confers resistance to α-specific PI3K inhibition

Fig. 5

p110β is activated in an IGF1R/IRS (insulin receptor substrate)-dependent manner and promotes resistance to BYL719. a Immunoblots of coimmunoprecipitated p110β, p110α, or p85 PI3K from lysates of parental and resistant cells treated for 24 hours with or without IC90 concentrations of BYL719 combined with or without 1 μM of AEW541. b Immunoblots of immunoprecipitated p85 PI3K antibody from lysates of parental and resistant cells treated for 24 hours with IC90 concentrations of BYL719 combined with or without 1 μM AEW541. c Proliferation of parental and resistant cells treated with vehicle (VHC), AZD6482 (1 μM), BYL719 (IC90), or a combination of BYL719 and AZD6482 for 9 days. Cell numbers were evaluated using the sulforhodamide B assay. Data are mean ± SEM (n >3, *P <0.01, **P <0.001). d Growth curves of MCF7 tumors from Balb-c nude mice treated with VHC, 25 mg/kg BYL719 (p110α inhibitor) daily, 75 mg/kg AEW541 (IGF1R inhibitor) daily, 100 mg/kg GSK2636771 (p110β inhibitor) daily, alone or in combination as indicated. Data are mean ± SEM (n >5, *P <0.001). IP immunoprecipitation, MCF7p MCF7-parental, MCF7r MCF7-resistant, T47Dp T47D-parental, T47Dr T47D-resistant

Back to article page
\