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. Author manuscript; available in PMC: 2019 Dec 1.
Published in final edited form as: Mol Cancer Ther. 2018 Sep 6;17(12):2710–2721. doi: 10.1158/1535-7163.MCT-18-0374

Figure 3. Inhibition of glutathione synthesis abrogates resistance to PI3K inhibitor.

Figure 3.

(A) The cellular levels of GSH and NADPH after treatment with buparlisib. EV and PIM1 expressing LNCaP cells were exposed to 1 μmol/L buparlisib for 48 hr. The data shown is the mean of measurements ± SD (n=4). *, P<0.05; n.s., not significant.

(B) Impact of buthionine sulfoxide (BSO) pretreatment on the sensitivity of LNCaP/PIM1 versus LNCaP/EV cells to 1 μmol/L buparlisib (72 hr). The data shown is the mean of measurements ± SD (n=4).

(C) Tumor volume of implanted LNCaP/PIM1 cells treated with the indicated agents for varying periods of time. The average volume ± SEM (n=6), and statistical comparison to the vehicle treated control is shown (*, P<0.05). The tumors shown were excised from the mice at the end of treatment.

(D) Fluorescence imaging of ROS in LNCaP/EV cells treated with buparlisib for 16 hr in presence of PBS, Trolox (1 mmol/L) or NAC (3 mmol/L) (scale bar, 20 μm). Quantitation of DCF green intensity following treatment with 1 μmol/L buparlisib. The average of these values ± the SD is shown.

(E) Fluorescence imaging of ROS in LNCaP/PIM1 cells treated with 1 μmol/L buparlisib for 16 hr in presence or absence of BSO (scale bar, 20 μm). The average value of ROS determined by DCF green florescence intensity and SD of these measurements is shown.