Bemcentinib inhibits cell growth and induces cell cycle arrest and apoptosis of MCL cells. (A-D) MCL cell lines were treated with the AXL inhibitor bemcentinib in concentrations ranging from 0 to 8 μM. The number of viable cells, as determined by trypan blue exclusion, decreased in a time- and dose-dependent manner. Experiments were performed in triplicates and the means ± standard deviations are shown. (E) Cell cycle analysis performed by flow cytometry revealed that inhibition of AXL activity induces a cell cycle arrest of MCL cells. Triplicate experiments were performed and a representative result for each MCL cell lines is shown. (F-G) The JeKo-1 and Granta-519 MCL cell lines were treated with different concentrations of bemcentinib. The number of dead cells was assessed by trypan blue exclusion. Bemcentinib treatment induced cell death in a dose-dependent manner. The experiments were performed in triplicates and the means ± standard deviations are shown. (H) Apoptosis was monitored by caspase activation in MCL cells (Mino, JeKo-1, and REC-1) treated with bemcentinib. Inhibition of AXL activity triggered apoptosis as revealed by PARP cleavage and caspase 3, 7, and 9 activation. (I) MCL cells were treated with various doses of bemcentinib and AKT acitvation was evaluated by western blotting. Inhibition of AXL induced a decrease in AKT activation. The experiments were performed in triplicates and a representative blot is shown. (J) AXL inhibition by bemcentinib decreased NF-κβ activation in MCL cell lines. NF-κβ activation was evaluated by western blot using a phospho-antibody. Quantification of NF-κβ activation is shown for each MCL cell lines. The experiments were performed in triplicates and the means ± standard deviations are shown. (K) The expression of β-catenin, cyclin D1, p-27, and GLUT-3 was investigated by western blot in JeKo-1 and REC-1 MCL cells. Bemcentinib treatment induced a dose-dependent decrease in β-catenin, cyclin D1, and p-27 expression. No decrease in GLUT3 was observed. The experiments were performed in triplicates and a representative blot is shown for each cell line.

Bemcentinib inhibits cell growth and induces cell cycle arrest and apoptosis of MCL cells. (A-D) MCL cell lines were treated with the AXL inhibitor bemcentinib in concentrations ranging from 0 to 8 μM. The number of viable cells, as determined by trypan blue exclusion, decreased in a time- and dose-dependent manner. Experiments were performed in triplicates and the means ± standard deviations are shown. (E) Cell cycle analysis performed by flow cytometry revealed that inhibition of AXL activity induces a cell cycle arrest of MCL cells. Triplicate experiments were performed and a representative result for each MCL cell lines is shown. (F-G) The JeKo-1 and Granta-519 MCL cell lines were treated with different concentrations of bemcentinib. The number of dead cells was assessed by trypan blue exclusion. Bemcentinib treatment induced cell death in a dose-dependent manner. The experiments were performed in triplicates and the means ± standard deviations are shown. (H) Apoptosis was monitored by caspase activation in MCL cells (Mino, JeKo-1, and REC-1) treated with bemcentinib. Inhibition of AXL activity triggered apoptosis as revealed by PARP cleavage and caspase 3, 7, and 9 activation. (I) MCL cells were treated with various doses of bemcentinib and AKT acitvation was evaluated by western blotting. Inhibition of AXL induced a decrease in AKT activation. The experiments were performed in triplicates and a representative blot is shown. (J) AXL inhibition by bemcentinib decreased NF-κβ activation in MCL cell lines. NF-κβ activation was evaluated by western blot using a phospho-antibody. Quantification of NF-κβ activation is shown for each MCL cell lines. The experiments were performed in triplicates and the means ± standard deviations are shown. (K) The expression of β-catenin, cyclin D1, p-27, and GLUT-3 was investigated by western blot in JeKo-1 and REC-1 MCL cells. Bemcentinib treatment induced a dose-dependent decrease in β-catenin, cyclin D1, and p-27 expression. No decrease in GLUT3 was observed. The experiments were performed in triplicates and a representative blot is shown for each cell line.

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