Fig. 2: The CDK1/2 inhibitor milciclib induces G1 arrest in T-ALL cell lines.
a Dose-response curves of milciclib treatment in 11 T-ALL cell lines. Cells were treated with increasing concentrations of milciclib (3.2 nM–32 µM range) in triplicate and cell viability was assessed after 72 h using the colorimetric MTT assay. Cell survival was calculated in comparison to the untreated control. Each point represents the mean and standard deviation of the triplicate. The green box shows the corresponding clinical concentration range of milciclib used in patients enrolled in clinical trials51. b Cell cycle analysis upon milciclib treatment. Cells were treated with either 100 nM or 1 µM milciclib for 72 h and cell cycle analysis was performed via Hoechst-DNA staining and FACS analysis. The graphs show the average and standard deviation of three independent experiments. Significance was determined using a paired, two-tailed Student’s t-test and annotated as “ns” (not significant, p ≥ 0.05), * (p < 0.05), ** (p < 0.01). c Detection of apoptotic cells upon milciclib treatment. Cells were treated with either 100 nM or 1 µM milciclib for 72 h and Annexin V/ Propidium Iodide (PI) staining was used to detect apoptosis. Apoptotic cells were identified as the sum of the Annexin V+ cells and Annexin V+/PI+ cells. The percentage of apoptotic cells is calculated compared to untreated control cells. The graphs show the average and standard deviation of three independent experiments. Significance was determined using a paired, two-tailed Student’s t-test and annotated as *(p < 0.05), **(p < 0.01), ****(p < 0.0001). If not annotated, the results were not significant (p ≥ 0.05). d Western blot analysis upon milciclib treatment. HSB-2 cells and P12-ICHIKAWA cells were treated with 100 nM milciclib for 72 h and 20 µg of protein was used for each condition. The image is representative of three independent experiments. Source data are provided as a Source Data file.
