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. Author manuscript; available in PMC: 2011 Sep 22.
Published in final edited form as: Cancer Res. 2010 Aug 10;70(17):6804–6814. doi: 10.1158/0008-5472.CAN-10-0409

Figure 2. Coexistent PIK3CA mutation is associated with decreased dependency on MEK signaling for tumor growth in vitro and in vivo.

Figure 2

A: Immunoblots showing the effects of MEK inhibition in PD0325901 sensitive (SW620, H747) and resistant (HCT-15, DLD-1) cell lines. Cells were treated with 50nM PD0325901 and lysates immunoblotted with the specified antibodies.

B: MEK-dependent (SW620, H747) and MEK-independent (HCT-15, DLD-1) cells were treated with 50nM PD0325901 or DMSO control and harvested 48 hours later. Graphs show: (Top) the percent of cells with G1 DNA content and (Bottom) the apoptotic fraction reported as the percent of cells with sub-G1 DNA content. The results represent the mean ± SE of two independent experiments done in triplicate.

C: MEK-dependent (SW620, H747) and MEK-independent (HCT-15, DLD-1) cells were treated with PD0325901 in a soft agar colony formation assay. Representative images at 21 days post plating are shown.

D: Mice with established SW620 and HCT15 xenografts were treated with PD0325901 × 5 days/week, for 3 weeks, or with vehicle only. The results represent the mean percent increase in tumor volume ± SE (n = 5 mice/group).