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. 2019 Feb 15;120(6):658–667. doi: 10.1038/s41416-019-0394-9

Fig. 2.

Fig. 2

ΔNp63α downregulation is required for the inhibitory activity of SAHA, which treatment decreases epidermal growth factor receptor (EGFR) expression. a Optical density (OD) analysis of the expression of ΔNp63α from three independent western blot experiments of head and neck cancer (HNC) cell lines treated with 5 μM SAHA or vehicle for 24 h was performed. Results were normalised to loading control (GAPDH) and expressed as percentage of inhibition (means ± SD). b Percentage of ΔNp63α inhibition results obtained in a were correlated to SAHA IC50, Pearson correlation coefficient r = −0.6 (P < 0.05). c HNC cell lines were treated with 2 or 5 μM SAHA or vehicle for 24 h, lysed and analysed by immunoblotting (IB) with the indicated antibodies. d HNC cell lines were treated with 5 μM SAHA or vehicle for 24 h, lysed and analysed by IB with the indicated antibodies. e, f OD analysis of the expression of EGFR from three independent western blot experiments of HNC cell lines, shown in d, treated with 5 μM SAHA or vehicle for 24 h was correlated to OD results of percentage of p63 inhibition mediated by SAHA (e) or SAHA IC50 (f). Pearson correlation coefficient r = 0.78 (P < 0.005) and r = −0.78 (P < 0.005) respectively. g UM-SCC-4 cell line was transduced with EGFR-encoding viral particle; puromycin-selected cells were treated with SAHA, gefitinib and the combination of the two drugs, and IC50 was assessed using CellTiter-Glo® Luminescent Cell Viability Assay