Fig. 3

PLK1i synergizes with KRAS^G12Ci via ERK-dependent and -independent downregulation of c-Myc. A Representative Volasertib and BI 2536 dose-response curves and IC₅₀ values of eight cell lines. B Volasertib inhibited the viability of Ba/F3 cells expressing KRAS^G12C, or KRAS^G12C second-site mutants. C Relative cell viability of MIA PaCa-2-R, NCI-H358-R and SW1573 cells treated with Volasertib (5 nM), KRAS^G12Ci (1 µM), or their combination for 72 h. D CI values of PLK1i in combination with KRAS^G12Ci were tested by cell viability assay and calculated by CalcuSyn software. E Clonogenic growth of cells treated with Volasertib (2 nM) or BI 2536 (1 nM) in combination with KRAS^G12Ci. Quantified results were shown. Cell cycle (F) and apoptosis analysis (G) of cells treated with PLK1i in combination with KRAS^G12Ci for 24 h. H Effects of Volasertib (20 nM), AMG510 (100 nM), or their combination (24 h) on histone H3 (Ser10) phosphorylation were shown by immunofluorescence in MIA PaCa-2-R cells. Scale bar, 5 μm. I Immunoblotting of cells treated with PLK1i in combination with AMG510 for 24 h. Data represent mean ± SD. Statistical significance was assessed using two-tailed unpaired Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001. See also Additional file 2: Fig. S4