Figure 1
From: NT157 exerts antineoplastic activity by targeting JNK and AXL signaling in lung cancer cells
NT157 reduces cell viability, clonogenicity and induces apoptosis in lung cancer cells. (a) Dose- and time-response cytotoxicity was evaluated by the sulforhodamine B (SRB) assay. H1299 and H460 cells were treated with vehicle (Ø) or different concentrations of NT157 (1.6, 3.2, 6.4, 12.5, 25, 50, and 100 µM) for 24, 48, and 72 h. Values are expressed as the percentage of viable cells for each condition relative to vehicle-treated cells. Results are shown as mean ± SD of at least 3 independent experiments. (b) Colony formation of the cells treated with vehicle or NT157 (1.6, 3.2, 6.4, and 12.5 µM) and for 7 days. The bar graph represents the mean ± SD of the relative number of colonies (% of control). ***p < 0.001; ANOVA and Bonferroni post-test. (c) Apoptosis was evaluated through annexin V/PI staining and flow cytometry. H1299 and H460 cells were treated with vehicle or NT157 (6.4 and 12.5 μM). Representative dot plots are shown for each condition; the upper and lower right quadrants (Q2 plus Q3) cumulatively contain the apoptotic population (annexin V + cells). **p < 0.01, ***p < 0.001; ANOVA and Bonferroni post-test. (d) Mitochondrial membrane potential analysis was evaluated using the JC-1 staining method and flow cytometry. Lung cancer cells were treated with vehicle or NT157 (6.4 and 12.5 μM). Note that NT157 increased the percentage of cells with disrupted mitochondrial membrane. Representative dot plots are shown for each condition; the gate FL-2 contains cells with intact mitochondria and the gate FL-2/FL-1 contains cells with damaged mitochondria. ***p < 0.001; ANOVA and Bonferroni post-test.
