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. 2024 Mar 13;43(19):1411–1430. doi: 10.1038/s41388-024-03000-9

Fig. 2. p53 loss drives MET inhibitor resistance in MPNSTs.

Fig. 2

A Percent viability of NF1-MET and NF1-MET;sgP53 cells after 72 h of capmatinib (100 nM), trametinib (40 nM) or combination (capmatinib 100 nM, trametinib 40 nM) treatment. B, C Western blot of NF1-MET and NF1-MET;sgP53 cells treated with capmatinib (100 nM) for 2 h and stimulated with HGF (B) or 10% FBS (C) for 15 min. Images (D) and flow cytometry analysis (E) of GFP labeled NF1-MET and RFP labeled NF1-MET;sgP53 cells after 3 and 5 days of treatment with vehicle (DMSO), capmatinib (100 nM), or trametinib (40 nM). F Individual tumor growth curves, LOESS curves, and 95% ribbons for vehicle or capmatinib (30 mg/kg BID) treated NF1-MET and NF1-MET;sgP53 xenografts. G Pairwise comparison of growth trend estimates in capmatinib treated NF1-MET (p-value = 0.0083) and NF1-MET;sgP53 (p-value = 0.089) tumors to 0 (grey line). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.