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. 2020 Feb 10;12(2):406. doi: 10.3390/cancers12020406

Figure 5.

Figure 5

WP1130 causes oxidative stress to activate stress-related p38/JNK MAPKs pathways and DNA damage responses to induce apoptosis. (A) HEL cells were treated for 6 h with or without 5 µM WP1130 and subjected to immunoblot analysis with antibodies against indicated proteins. ß-actin was used for a loading control. (B) HEL cells were left untreated as control (Cont.) or treated for 3 h with 3 μM WP1130 (WP), 3 μM G9, and 5 mM NAC, as indicated, and analyzed for reactive oxygen species (ROS) by flow cytometry. (C) HEL cells left untreated or pretreated with 40 mM NAC for 1 h were further treated with 5 μM WP1130 for indicated times and analyzed by immunoblot analysis. The results obtained from duplicate gels are shown above or below a thin horizontal line. (D) Primary post-MPN sAML cells expressing JAK2-V617F were treated with 5 μM WP1130 for indicated times and analyzed. An arrow indicates the position of cleaved PARP. (E) HEL cells were left untreated as control or treated for 24 h with 3.5 μM WP1130 and 5 mM NAC, as indicated, and analyzed for DNA content. Percentages of apoptotic cells with the sub-G1 DNA content are indicated. (F) HEL cells were left untreated as control or treated for 24 h with 3.5 μM WP1130, 50 μM SB203580, and 50 μM SP600125, as indicated, and analyzed.