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. 2019 Jan 22;11:1023–1032. doi: 10.2147/CMAR.S187597

Figure 5.

Figure 5

Depletion of thioredoxin sensitizes AML to ETP treatment.

Notes: (A–C) HL60 cells transfected with siCtrl or siTrx1 were treated with vehicle control (Ctrl) or 2 µM ETP for 48 hours. (A) The protein expression of Trx1 was determined by Western blot. GAPDH was used as a loading control. The representative images (left) and the quantification of band intensity (right) are shown. (B) The intracellular ROS level was detected by flow cytometry analysis using DCFH-DA. Results relative to Ctrl are shown. (C) Cell viability was determined via trypan blue exclusion assay. Results relative to Ctrl are shown (%). Data were obtained from at least three independent experiments and analyzed by Student’s t-test. Data are presented as mean ± SD. **P<0.01. (D) Brief schematic graph of a model for the role of HHT in augmenting ETP cytotoxicity in AML cells through targeting thioredoxin-mediated ROS elimination.

Abbreviations: AML, acute myeloid leukemia; DCFH-DA, dichlorofluorescein diacetate; ETP, etoposide; HHT, homoharringtonine; NS, not significant; ROS, reactive oxygen species.