* * * A B D C E CP110 Tubulin WB: CP110 WB: HA CP110 KRAS Tubulin

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* * * A B D C E CP110 Tubulin WB: CP110 WB: HA CP110 KRAS Tubulin Supplemental Fig. S4 A CP110 Tubulin WB: CP110 WB: HA B * % Growth * * D CP110 KRAS siRNA2 Control KRAS siRNA1 Control KRAS siRNA1 KRAS siRNA2 KRAS Tubulin Seliciclib (µM) C CP110 E Actin CP110 ED1 344P 393P LKR13 KRAS KRAS siRNA1 KRAS siRNA2 KRAS Tubulin Control Control KRAS siRNA1 KRAS siRNA2 Actin ED1 344P 393P LKR13 Supplemental Fig. S4. (A) Effect of engineered KRAS expression on response to CDK2 inhibition by seliciclib. KRAS mutation sensitized lung cancer cells towards seliciclib-mediated CDK2 inhibition of growth as compared to control-ED-1 cells. (B) Cells transfected with the plasmid expressing HA-tagged human CP110 were used for detection of CP110 using an anti-CP110 antibody (1:1000) and an anti-HA antibody (1:1000), respectively. The upper band detected by the anti-CP110 antibody specifically recognizes CP110. (C) Respective CP110 and RAS protein expression profile in murine lung cancer cell lines is shown. (D) Effect of KRAS knockdown at 48 hours (left panel) and 72 hours (right panel) on CP110 expression in the 344P cell line. (E) Effect of KRAS knockdown at 72 hours (left panel) and 96 hours (right panel) on CP110 expression in the Hop62 cell line. * P < 0.05