Figure 4From: Genetic targeting of B-RafV600E affects survival and proliferation and identifies selective agents against BRAF-mutant colorectal cancer cellsChemosensitivity for B-Raf inhibitors. A: Multi-kinase inhibitor sorafenib had no differential effect on RKO BRAF knockout cell clones. B-C: Although no significant differences in the IC50 were observed, by trend RBW-1 was less sensitive to vemurafenib and RAF265 compared to cells with mutant BRAF alleles. D: The IC50 of the B-Raf kinase inhibitor dabrafenib in RBW-1 was 5.3 times higher than the IC50 of the parental clones RKO-E1 and RBOW, and 20 times higher than in clones carrying a BRAF-mutant allele only. E: Aliquots of each cell line were incubated with the respective IC50 concentrations of B-Raf inhibitors, lyzed, and analyzed in Western blots for phosphorylation of Mek 1/2 (upper panel) and Erk 1/2 (lower panel). F: Signal intensities of phospho-Mek 1/2 and phosphor-Erk 1/2 were normalized to the total fractions in densitometric analyses.Back to article page