Fig. 3: ET reduced RON/PI3K pathway activation.
From: RON signalling promotes therapeutic resistance in ESR1 mutant breast cancer

a Fold change of kinases in KiP analysis in MCF-7 Y537S cells after treatment with Tam. X-values represent fold change of Tam-treated Y537S cells compared to untreated Y537S cells. b MCF-7 cells were cultured in 10% FBS supplemented media and treated with 1 µM Tam and 1 µM Ful for 48 h. Immunoblot analysis of phosphorylated and total RON was performed. Numbers below each protein represent normalised densitometry of each protein compared to GAPDH. c MCF-7 cells were cultured in 10% FBS supplemented media and treated with Tam and Ful for 48 h. qRT-PCR analysis of RON was performed. Graphs represent mean + standard error of the mean (N = 3 replicates). Two-way ANOVA was used for statistical analysis. d MCF-7 cells were cultured in 10% FBS supplemented media and treated with RONi for ninety minutes. Immunoblot analysis was performed for phosphorylated and total AKT and p44/42 MAPK. e MCF-7 cells were cultured in charcoal-stripped serum supplemented media and treated with RONi for 24 hours and ER transactivation assay was performed. Graphs represent mean + standard deviation (N = 3 replicates). Student’s t-test was used for statistical analysis. f MCF-7 cells were cultured in 10% FBS supplemented media and treated with 1 µM Tam and 1 µM Ful for 48 h. Immunoblot of phosphorylated and total AKT and p44/42 MAPK was performed. g T47D cells were cultured in 10% FBS supplemented media and treated with Tam and Ful for 48 h. Immunoblot of phosphorylated and total AKT and p44/42 MAPK was performed. P < 0.05 was considered statistically significant in all tests. (*p < 0.05, **p < 0.01, ***p < 0.001).