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. 2018 Sep 24;9(10):976. doi: 10.1038/s41419-018-1034-7

Fig. 1. The STAT1:ERK1/2 signaling ratio downstream of EGFR is altered in metastatic cells compared to primary breast cancer cells.

Fig. 1

a Schematic representation of the EGFR-transformed lung-metastatic breast cancer progression series. b Cells described in panel a were analyzed by immunoblot for phosphorylation of STAT1 and ERK1/2 in response to a 30 min EGF stimulation (50 ng/ml). IL6 and BSA (0) served as protein stimulation controls, and analysis of total levels of EGFR, STAT1, ERK1/2, and Actin served as loading controls. c Non-metastatic (NME) and lung metastatic (NME-LM1) cells as described in panel a were stimulated for 30 min with the indicated concentrations of EGF and analyzed for phosphorylation of STAT1. Analysis of total STAT1 served as a loading control. d Schematic representation of the EGFR-transformed lymph node-metastatic breast cancer progression series. Metastatic cells were isolated from two separate lymph-nodes and termed NME-Lym1 and NME-Lym2. e Cells described in panel d were analyzed for phosphorylation of STAT1 and ERK1/2 in response to a 30 min EGF stimulation (50 ng/ml). IL6 and BSA served as stimulation controls, and analysis of total levels of EGFR, STAT1, ERK1/2, and Actin served as loading controls. f EGFR was ectopically expressed in metastatic MCF10-Ca1a cells. These cells were stimulated with EGF (50 ng/ml) for 30 min and analyzed for phosphorylation of STAT1 and EGFR. Analysis of total levels of EGFR and STAT1 served as loading controls. All immunoblots shown are representative of at least three independent experiments