Figure 5.

GPX1 could mediate cisplatin resistance in NSCLC via the PI3K-AKT pathway. (a) Treatment of GPX1 downregulated A549 cells with EGF, a PI(3)K activator, increased their sensitivity to cisplatin compared to A549 cells treated with siGPX1 alone. Western blot analysis demonstrating an inhibition of AKT phosphorylation in response to LY294002 in GPX1-downregulated A549 cells and regaining the expression of that by treatment of EGF. (b) Treatment of GPX1 upregulated H1650 cells with LY294002, a PI(3)K inhibitor, decreased their sensitivity to cisplatin compared to H1650 cells treated with GPX1 vector alone. (∗: LY294002a, LY294002 with siGPX1; EGFa, EGF with siGPX1; LY294002b, LY294002 with GPX1 vector; EGFb, EGF with GPX1 vector.)