Fig. 3
a Panobinostat and erlotinib cooperate in reducing the abundance of phospho-EGFR in NSCLC cell lines. Western Blot analysis of the TKI-sensitive cell line HCC827 and the TKI-insensitive cell lines A549 and NCI-H460 was performed using antibodies against the phosphorylated EGF-receptor and, serving as control, total EGFR. b Panobinostat and erlotinib differentially regulate phospho-AKT and phospho-ERK. Western blot analysis of the proliferation and survival promoting proteins of the MAPK-pathway: phospho-ERK (compared to total ERK), and of the PI3K-pathway: phospho-AKT (compared to total AKT). c Regulation of cell cycle proteins p21WAF1/CIP1, p53 and CHK1 by panobinostat and erlotinib combination treatment. Western blot analysis after 24, 48 and 72 h of treatment with PS and/or erlotinib was performed using antibodies against p21WAF1/CIP1, p53, phosphorylated CHK1 (Ser280) and total CHK1. An induction of p21WAF1/CIP1 and p53 after PS as well as combination treatment was detectable in both EGFR wt cell lines A549 and NCI-H460 only. A downregulation of CHK1 after PS and combination treatment was seen in all three cell lines. d Panobinostat alone and in combination with erlotinib upregulates E-Cadherin and β-catenin in the EGFR wildtype NSCLC adenocarcinoma cell line A549. Western blot analysis of the three NSCLC lines after 24, 48 and 72 h of combination treatment was performed using antibodies against E-Cadherin and β-Catenin