Fig. 5

Combining panobinostat with inhibition of EGFR leads to enhanced apoptosis induction. A Effect of panobinostat at 16 nM for A204, 25 nM for VAESBJ and 60 nM for GRU1, corresponding to the IC₅₀ as measured previously by MTS, with other anticancer agents on cell proliferation (427 nM of pazopanib for A204, as measured previously by MTS). Results determined by MTS assay in N ≥ 3 biological replicates (non-parametric Kruskal-Wallis test, A204 p = 0.0037, VAESBJ p = 0.0013, GRU1 p = 0.0014), graph represents means ± SEM. B Decrease of cell proliferation induced by panobinostat at the respective IC₅₀ as indicated above with erlotinib at different dose levels after 72 h, by MTS in N ≥ 3 biological replicates (non-parametric Kruskal-Wallis test, A204 p = 0.0027, VAESBJ p = 0.0051, GRU1 p < 0.0001), graph represents means ± SEM. C Cells were treated for 24 h with panobinostat at the respective IC₅₀ as indicated above in combination with different dose levels of erlotinib; activation of ERK and AKT as well as PARP cleavage was assessed by Western blot