Fig. 2: CUTO44 cell line is resistant to single-agent EGFR inhibition but sensitive to combination with crizotinib or trametinib.
From: Evolution of MET and NRAS gene amplification as acquired resistance mechanisms in EGFR mutant NSCLC
a MET FISH analysis of the patient tumor sample upon progression on erlotinib (left) and the CUTO44 cell line (derived from the same biopsy, right) showing MET probes labeled in red and the chromosome 7 centromere probes in green. b Cell proliferation inhibition following treatment with erlotinib, afatinib, or osimertinib. CUTO44 cells were treated with the indicated concentration of drugs for 72 h and proliferation was measured by MTS assay. Showing the mean ± SD, n = 3 biological replicates. c Western blot showing downstream signaling changes following treatment with EGFR inhibitors and crizotinib. CUTO44 cells were treated with the indicated drugs for 2 h before lysis and protein analysis by western blot. Showing representative images, n = 2. d Cell proliferation following treatment with crizotinib and the combination with EGFR inhibitors. Same as in b. e Cell proliferation inhibition of cells treated with trametinib and the combination with EGFR inhibitors. Same as in b. f Western blot showing downstream signaling changes following drug combination treatments. Same as in c with drugs combined at the indicated doses.
