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. 2016 Nov 7;7(52):85917–85928. doi: 10.18632/oncotarget.13185

Figure 2. Antagonism of Dex on gefitinib-induced apoptosis in NSCLC cells.

Figure 2

(A) PC9 (EGFRexon19del E746-A750) cells were treated with vehicle control (DMSO), gefitinib at 200 nM (IC80), or gefitinib with Dex (1 μM) or RU486 (1 μM). Cell apoptosis was evaluated by apoptosis assay after 48 hours of drug treatment. The percentages of apoptotic cells in each treatment group are shown in the histogram. Three repeating assays were performed. ***p < 0.001 compared to VC; ###p < 0.001. (B) NCI-H1975 (EGFRL858R/T790M) cells were treated with the drug combinations described for panel (A), except the 200 nM gefitinib was replaced with 500 nM afatinib. Three repeating assays were performed. **p < 0.01 and ***p < 0.001 compared to VC; ###p < 0.001. (C) PC9 cells were treated with drugs as described in panel (A) for 48 hours and then analyzed for mitochondria membrane potential (MMP), as indicated by % Δψm. Three repeating assays were performed. ***p < 0.001 compared to VC; ###p < 0.001. (D) NCI-H1975 cells were treated with drugs as described in panel (B) for 48 hours and then analyzed for mitochondria membrane potential (MMP), as indicated by %Δψm. Three repeating assays were performed. ***p < 0.001 compared to VC; ###p < 0.001. Abbreviations: VC, vehicle control; Gefi, gefitinib only; Dex, dexamethasone.