Fig. 3

UNC2250 reduced activation of downstream signaling and inhibited proliferation and invasion of MCL cells. a UNC2250 induced suppression of MerTK-dependent signaling pathways in a dose-dependent manner. Z-138, Mino, and JVM-2 cells were treated with indicated concentrations of UNC2250 for 60 min; then, whole cell lysates were detected by western blot for phospholated and total MerTK, AKT, and p38. b UNC2250 inhibited proliferation of MCL cells in a dose-dependent manner. Cells were cultured in the absence (vehicle) or presence (dosing) of UNC2250 for 72 h. Viable cells were measured by Cell Titer-Glo Luminescent Cell Viability Assay system. Inhibition rates were calculated by (1 − dosing/vehicle) × 100%. c UNC2250 suppressed invasion of Z-138, Mino, and JVM-2 cells in a dose-dependent manner. Z-138, Mino, orJVM-2 cells pre-treated with vehicle and 2 or 4 μM UNC2250 for 2 h were seeded into transwell chambers coated with Matrigel inserted in 24-well plates. Invasive abilities were determined by viable cells invading into the lower chamber. Images from a representative experiment are shown. Mean values and SEs were derived from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. d UNC2250 mediated decreases of phospholated FAK and total RhoA in a dose- and time-dependent manner in Z-138 and Mino cells. Cells were treated with indicated concentrations of UNC2250 for 2 or 12 h; then, whole cell lysates were detected by western blot for phospholated FAK and total RhoA. Actin is shown as a loading control