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. 2020 Dec 23;107(1):58–76. doi: 10.3324/haematol.2020.260331

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Figure 3. — MCL-1 expression contributes to venetoclax resistance, and the combined inhibition of BCL- 2 and MCL-1 synergistically induces apoptosis in acute myeloid leukemia cells with intrinsic or acquired resistance to venetoclax. (A and B). Control (con) and MCL-1 knockdown (MCL-1-KD) OCI-AML3 cells (A) or control and MCL-1 overexpressing (MCL-1-OE) Molm13 cells (B) were treated with venetoclax (VEN) or AZD5991 for 48 hours (h). (C to E) OCI-AML3 (C), MCL-1-OE Molm13 (D), and control parental MV4-11 cells (MV4-11P) or venetoclax- resistant MV4-11 cells (MV4-11R) (E) were treated with venetoclax and/or AZD5991 for the indicated times. Apoptosis and viable cell numbers were assessed by flow cytometry. Experiments were performed in triplicates. Results are expressed as the mean ± standard error of the mean. IC₅₀: half maximal inhibitory concentration; EC₅₀: half maximal effective concentration; CI: combination index; OE: overexpressing; KD: knockdown.