Fig. 4

ML385 cooperates with FIN56/RSL3 to induce the cell death of AML cells. (a) MV4;11 (upper panel) and Kasumi-1 cells (lower panel) were treated with 0.5 µM RSL3, 5 µM ML385, or the combination of RSL3 and ML385 for 24 h, and the percentage of Annexin V + cells was determined by flow cytometry. (b) MV4;11 (upper panel) and Kasumi-1 cells (lower panel) were treated with 10 µM FIN56, 10 µM ML385, or the combination of FIN56 and ML385 for 48 h, and the percentage of Annexin V + cells was determined by flow cytometry. (c) MV4;11 cells were co-treated with RSL3 and ML385 (upper panel) or with FIN56 and ML385 (lower panel) at the indicated concentration for 24 h, and the cell cycle was determined by flow cytometry. (d) BMMCs from newly diagnosed AML patients were treated with 2 µM RSL3, 10 µM ML385, or a combination of RSL3 and ML385 for 48 h (upper panel), as well as with 10 µM FIN56, 10 µM ML385, or a combination of FIN56 and ML385 for 48 h (lower panel), and cell viability was analyzed using the CCK8 assay. (e) BMMCs from newly diagnosed AML patients were treated with 2 µM RSL3, 10 µM ML385, or a combination of RSL3 and ML385 for 48 h (upper panel). In addition, cells were treated with 10 µM FIN56, 10 µM ML385, or a combination of FIN56 and ML385 for 48 h (lower panel). The percentage of Annexin V + cells was then detected using flow cytometry. Data are expressed as the mean ± SD. n = 3 or more independent biological replicates, presented as individual points. P value < 0.05 was considered significant (a-e, one-way ANOVA with Bonferroni post hoc test).