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. Author manuscript; available in PMC: 2011 Jan 19.
Published in final edited form as: Cancer Cell. 2010 Jan 19;17(1):77–88. doi: 10.1016/j.ccr.2009.11.022

Figure 1. HCC827 PFR cells are resistant to PF00299804, but combined MET and EGFR inhibition blocks PI3K/AKT and ERK signaling and restores sensitivity in vitro and in vivo.

Figure 1

(A) Parental and resistant HCC827 PFR5 cells treated with increasing concentrations of PF00299804. Cell viability relative to untreated controls measured after 72 hours. Each data point represents the mean ±SD of 6 wells. (B) HCC827 and HCC827 PFR5 and PFR6 cells were treated for 6 hours with 1 μM PF00299804 or gefitinib, PHA-665,752, or their combination. Cell lysates were immunoblotted to detect indicated proteins. (C) Upper, HCC827 PFR6 cells treated with increasing concentrations of PF00299804, PF2341066, or their combination. Lower, HCC827 PFR6 cells treated with increasing concentrations of gefitinib alone or in combination with PF2341066. Cell viability relative to untreated controls measured after 72 hours. Each data point represents the mean ±SD of 6 wells. (D) HCC827 PFR xenogafts in nu/nu mice were treated with PF2341066, PF00299804, or their combination. Tumors measured twice weekly. Only combination treatment led to tumor shrinkage and was the most effective treatment in vivo (p < 0.0001). Treatment was stopped after 56 days (arrow) and no tumor re-growth was observed in 35 weeks. Each data point represents the mean ±SD for 5 mice.