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. 2012 Feb 2;7(2):e30820. doi: 10.1371/journal.pone.0030820

Figure 1. Erlotinib fails to inhibit STAT3 activation in EGFR mutant NSCLC cell lines.

Figure 1

A–B, Protein lysates from HCC827 (A) and HCC4006 (B) cells treated with DMSO (vehicle) or 2 µM erlotinib for 8 hours were analyzed with antibody microarrays to detect phosphorylation status of receptor tyrosine kinases and key cell signaling proteins. Fluorescent signals for the indicated spots were background subtracted and normalized to positive control spots (indicated with +) on the array. Data is shown as the percentage of average fluorescence for each set of duplicate spots relative to the average fluorescence of ten positive control spots for each array. Data on each graph is ordered according to the number (1–10) indicated on each array. C, HCC827 and HCC4006 cells were treated for one hour with DMSO (con) or a 2-fold escalating dose of erlotinib ranging from 0.25 to 1.0 µM (left-right). The phosphorylation status of EGFR (pEGFRY1068), STAT3 (pSTAT3Y705), AKT (pAKTS473), ERK (pERKT202/Y204), and S6 (pS6S235/S236) was evaluated by immunoblot. Equal amounts of protein (20 µg) were added for each sample. D, HCC4006 cells were treated for two hours with DMSO or 1.0 µM erlotinib, then fixed and stained with antibodies for total STAT3. Cells were counter-stained with DAPI to indicate nuclear accumulation of STAT3. Scale bars, 20 µm.