Fig. 1: Acquired venetoclax-resistant hematologic cell lines possess higher intracellular O2.− and Mcl-1 levels. | Leukemia

Fig. 1: Acquired venetoclax-resistant hematologic cell lines possess higher intracellular O2.− and Mcl-1 levels.

From: Superoxide-mediated phosphorylation and stabilization of Mcl-1 by AKT underlie venetoclax resistance in hematologic malignancies

Fig. 1

A Cell viability of venetoclax-sensitive (VEN-S) MOLM14, OCI-AML2, and acquired venetoclax-resistant (VEN-R) MOLM14 and OCI-AML2 cells following treatment with increasing concentration of venetoclax (VEN) for 48 h. Cell viability was measured using MTT assay. N = 3. B Western blot analyses showing Mcl-1, S70pBcl-2, Bcl-2, and Tubulin/β-Actin levels in MOLM14, OCI-AML2, OCI-Ly1 of VEN-S/parental or VEN-R cells, and TMD8 (inherently resistant) cells. N = 3. C Representative graph showing the kinetics of oxygen consumption rate (OCR) when MOLM14 and OCI-AML2 of VEN-S and VEN-R cells were subjected to oligomycin (1 µM), FCCP (1 µM), and rotenone/antimycin A (Rot/AA) (0.5 µM/0.5 µM) injection at the indicated timepoints of the assay. D Graph showing fold change in oxygen consumption rate (OCR) of MOLM14 and OCI-AML2 of VEN-S and VEN-R cells. OCR was measured via Seahorse assay (Agilent, USA). N = 3. Unpaired t-test was used. E Graph showing fold change in intracellular O2.− levels of MOLM14 (N = 4), OCI-AML2 (N = 3), OCI-Ly1 (N = 3) of VEN-S and VEN-R cells. Unpaired t-test was used. F Cell viability of VEN-S OCI-AML2 and inherently VEN-R OCI-AML3 cells following treatment with increasing concentrations of VEN (µM) for 48 h. Cell viability was measured via MTT assay. N = 3. Sidak’s multiple comparisons test was used. G-H Graph showing fold change in intracellular O2.− levels of inherently VEN-R OCI-AML3 or TMD8 cells relative to VEN-S OCI-AML2 or OCI-Ly1 cells, respectively. N = 4. Unpaired t-test was used. *MOLM14 and VEN-S MOLM14 or OCI-Ly1 and VEN-S OCI-Ly1 are used interchangeably.

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