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. Author manuscript; available in PMC: 2011 Jul 15.
Published in final edited form as: Cancer Res. 2010 Jun 22;70(14):5901–5911. doi: 10.1158/0008-5472.CAN-10-0192

Figure. 5. MEK-dependence of A146T KRAS mutant cell lines.

Figure. 5

A. IC50 values for the selective MEK1/2 inhibitor PD0325901 for thirty-five colorectal, lung and breast cell lines including all seven models harboring exon 4 KRAS mutation (4 A146T, 2 A146V and 1 K117N). B. Representative IC50 curves for the LS1034 (A146T KRAS), C80 (A146V KRAS), CCCL-18 (A146T KRAS, PIK3CA E542K), HCT-15 (KRAS G13D, PIK3CA E545K) and COLO-205 (V600E BRAF) models. C. Treatment of A146T KRAS expressing cell lines with PD0325901 was associated with a decrease in pERK and cyclin D1 expression, induction of p27 and hypo-phosphorylation of RB. (D). Cell lines expressing exon 4 KRAS mutations were resistant to the EGFR inhibitor gefitinib. The gefitinib-sensitive H3255 (L858R EGFR) model is included for comparison.