Fig. 4
From: Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC
EGFR TKI treatment increase β-catenin protein stability. a Cells were treated as described in Fig. 3 and were analyzed for the expression of total and non-phospho (active) β-catenin by WB using an antibody that recognizes the active form of β-catenin. b Cells were treated as described in Fig. 4 and prior to harvesting, cells were further treated with cycloheximide for the indicated times. Cell lysates were analyzed for non-phospho (active) β-catenin by western blot. c Western blots were quantitated and data plotted (trend line) as percentage of non-phospho β-catenin remaining as a function of cycloheximide treatment. d HCC827 cells were treated with erlotinib or DMSO and subjected to cytoplasmic and nuclear fractionation. Equal amounts of total protein from each fraction was analyzed for β-catenin (active, inactive, and total), Notch3, β-tubulin, and HDAC2. Error bars represent SD from biological triplicates
