An Acetamide Derivative as a Camptothecin Sensitizer for Human Non-Small-Cell Lung Cancer Cells through Increased Oxidative Stress and JNK Activation

Figure 6

The CPT and NPOA cotreatment induced apoptosis through activating JNK activity. The cells were subject to treatment with vehicle control or the indicated concentration of CPT and NPOA alone or in combination for 24 h and 48 h, respectively. (a) Western blot showed that the CPT and NPOA cotreatment significantly increased levels of JNK phosphorylation (Thr¹⁸³/Tyr¹⁸⁵) for 48 h. (b) The photograph showed the JC-1 green fluorescence image and indicated that SP600125 (SP) rescued the loss of mitochondrial membrane potential of H1299 cells after CPT and NPOA cotreatment. (c) The effect of SP600125 on CPT and NPOA cotreatment-induced JNK activation in H1299 cells was determined using flow cytometer-based detection assay. The cells were pretreated with JNK inhibitor SP600125 for 3 h and then subject to the treatment of CPT and NPOA alone or their combination. (d) The quantitative analysis of (c). Data are presented as means ± SD (). Abbreviations: p-JNK indicates phosphorylation-ERK; t-JNK indicates total-ERK. SP indicates SP600125, a JNK inhibitor. GAPDH was measured as an internal control.

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