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Fig. 3 | Molecular Medicine

Fig. 3

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

Fig. 3

Effect of mTOR overexpression and Evr treatment on the apoptosis of GEMsen and GEMres cells. a Flow cytometry of apoptosis in GEMsen and GEMres cells with or without ov-mTOR transfection or/and Evr treatment. Numbers in the upper right quadrant denote the percentage of cells in late apoptosis. b Quantification of the proportion of late-apoptotic cells. The numbers in the arrows represent the difference (increase or decrease) in the percentage of late apoptosis between ov-mTOR and ov-mTOR + Evr. In ov-mTOR-transfected GEMres cells, the enhancing effect of Evr on apoptosis was stronger than that in ov-mTOR-transfected GEMsen cells. c Ratio of the apoptosis of GEMres cells to that of GEMsen cells. d Western blot of proteins associated with apoptosis. Quantification of the protein expression of e Bax, f Bcl-2, and g Cyt-c in GEMsen and GEMres cells with or without ov-mTOR transfection or/and Evr treatment, normalized to that of GAPDH as an internal control. From e to g, the numbers in the arrows represent the difference (increase or decrease) in protein expression between ov-mTOR and ov-mTOR + Evr. In ov-mTOR-transfected GEMres cells, the overall enhancing effect of Evr on apoptosis was stronger 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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