Fig 1: The impact of TPD therapy on HER2+ breast cancer cells is contingent on the presence of S100-A11 in the CM secreted by CAF-200. A. The initial reduction in proliferation rates in the BT-474 cell line by TPD was attenuated by the addition of CAF-200–CM; however, this effect was less pronounced after S100A11 gene silencing in CAF-200 fibroblasts. CM [CAF-200] was obtained from CAF-200 treated with TPD under the indicated conditions (siC or siS100A11). The same effect was observed in the EFM-192A cell line. Treatment for 5 days with TPD therapy (15 μg/ml T; 20 μg/ml P; 0.5 and 1 nM D, respectively). Basal: control without recombinant protein; CM [CAF-200]: CAF-200–CM; siC: control silencing; siS100A11: silencing of S100A11 gene. (*): p < 0.05; (**): p < 0.01; (***): p < 0.001. Error bars represent the calculated value of the standard deviation (n = 6). B. WB analysis of BT-474 and EFM-192A cells, respectively, of phosphorylated and total forms of STAT3, AKT, and ERK proteins. The effect of the CAF-200–CM obtained after S100A11 gene silencing in CAF-200 fibroblasts was assessed for 6 h. Relative abundance levels of up- or down-regulated proteins were determined by densitometric analysis of the images, normalising them to β-actin loading control and to the respective untreated control. All immunoblot comparisons were performed within the same membrane and exposure conditions; therefore, signal intensities should not be compared across different figures. Representative images are shown for n = 3. Other specific details of the experimental conditions are shown in the Fig. 1 legend, unless otherwise indicated.