Supplemental Figure 1 from CDK2 Inhibition Causes Anaphase Catastrophe in Lung Cancer through the Centrosomal Protein CP110

Supplemental Fig. S1. Effect of wild-type or a phosphorylation sites mutant CP110 species on responses to CDK2 inhibition. (A) Overexpression of CP110 was detected in ED-1 cells with an anti-HA antibody 24 and 48 hours after transfection. (B) Overexpression of wild-type CP110 significantly reduced apoptosis induced by seliciclib treatment. ED-1 cells overexpressing CP110 were treated with the indicated dosages of seliciclib for 24 hours and analyzed for apoptosis. (C and D). Overexpression of phosphorylation-site mutated CP110 did not have a significant effect on anaphase catastrophe or apoptosis induced by CDK2 inhibition. ED-1 cells overexpressing a mutant-CP110 species were treated with the indicated dosages of seliciclib for 24 hours or transfected individually with two different siRNAs targeting CDK2 for 24 hours and (C) scored for multipolar anaphase and (D) analyzed for apoptosis. (E). Seliciclib treatment did not appreciably affect CP110 basal levels in human and murine lung cancer cells. Hop62 and ED-1 were treated with various dosages of seliclcib and CP110 levels were examined after 24 and 48 hours of treatment.