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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: Clin Cancer Res. 2012 Dec 18;19(3):657–667. doi: 10.1158/1078-0432.CCR-11-1446

Figure 6. Secondary resistance to PLX4720 is associated with increased expression of EGFR and activated AKT.

Figure 6

A. HT29 and Colo205 parental (P) and resistant (R) cells were plated overnight and then treated with various doses of PLX4720. Cells were trypsinized 72 h later, and viable cells were counted. (See also Supplemental Figure 4) B. Resistant clones (RC) of HT29 and Colo205 were cultured in drug-free media for 24 hours, the treated with 1 µM PLX4720 for 2 hours. C. Individual gene probes from a SNP tiling array for EGFR (n=145 probes) and KRAS (n=27 probes) were determined for HT29, Colo205, and their resistant clones. mRNA levels for EGFR and KRAS in the resistant clones were obtained as described in the methods and normalized to mRNA levels in the parental lines (which were set to a value of 1) D. Resistant clones of HT29 and Colo205 were cultured in drug-free medium for at least 24 h, and then cell lysates were prepared and subjected to immunoblot analysis to show expression of indicated proteins.