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. 2018 May 1;9(33):23058–23077. doi: 10.18632/oncotarget.25208

Figure 10. Combined EGFR and HER3 blockade sensitizes Th1 cytokine resistant triple negative breast cancer cells to senescence and apoptosis induction.

Figure 10

(A) Densitometric analysis presented as % of SA-β-gal-positive HCC-1143 cells transfected with non-target (NT) or EGFR and HER3 siRNA, untreated or treated with 200 ng/ml TNF-α (T) and 2000 U/ml IFN-γ (Ι), mean ± SD (n = 3), ***p < 0.001. Inset: HCC-1143 cells transfected with non-target (NT) or EGFR and HER3 siRNA probed with EGFR and HER3 specific antibodies. Vinculin was used as loading control. Representative data from 1 of 3 independent experiments. (B) Expression of p15INKb or cleaved caspase-3 in cells described in A. Vinculin was used as loading control. Similar results were observed in three independent experiments. (C) HCC-1143 cells were transfected with non-target (NT) or EGFR and HER3 siRNA, untreated or treated with 200 ng/ml TNF-α and 2000 U/ml IFN-γ for 5 min. EGFR and HER3 expression, phospho-Stat1 serine 727 and phospho-p38 MAPK threonine 180/tyrosine 182 were determined by western blot. Vinculin was used as loading control. Similar results were observed in three independent experiments. KD denotes knocked down. (D) Expression of phospho-Stat1 tyrosine 701 and p16INK4a proteins were detected in HCC-1143 cells treated with 200 ng/ml cetuximab for 48 hours followed by 200 μg/ml TNF-α and 2000 U/ml IFN-γ for 5 minutes. β-actin was used as loading control. Similar results were observed in 3 sets of independent experiments.