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Fig. 4 | Molecular Medicine

Fig. 4

From: Everolimus regulates the activity of gemcitabine-resistant pancreatic cancer cells by targeting the Warburg effect via PI3K/AKT/mTOR signaling

Fig. 4

Effect of mTOR overexpression and Evr treatment on PI3K/AKT/mTOR signaling in GEMsen and GEMres cells. a Western blot and quantification of the phosphorylation level of AKT and PI3K, normalized to that of GAPDH as an internal control. b Western blot and quantification of the phosphorylation level of mTOR (at S2481 and S2448) and P70S6K. The numbers in the arrows represent the difference (increase or decrease) in protein expression between ov-mTOR and ov-mTOR + Evr. The effect of Evr on the phosphorylation of AKT and mTOR (S2481) was similar between ov-mTOR-transfected GEMsen and GEMres cells. However, Evr exerted an overall stronger suppressive effect on the phosphorylation of PI3K, mTOR (S2448), and P70S6K in ov-mTOR-transfected GEMres cells than that in ov-mTOR-transfected GEMsen cells. The data are expressed as the mean ± standard deviation of three replicates (n = 3). *P < 0.05; #P < 0.05 compared with the same treatment in GEMsen cells. GEM: gemcitabine, Evr: everolimus; GEMsen: GEM-sensitive pancreatic cancer cells; GEMres: GEM-resistant pancreatic cancer cells; au: arbitrary units

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