FIGURE 2.

Effects of investigated inhibitors on the in vitro proliferation and apoptosis of HNSCC cell lines. (A,B) While therapeutic antibody cetuximab had no effect on in vitro cell proliferation in any of the two cell lines, small molecule EGFR- and c-MET-specific TKIs and RAS inhibitors were found to be more effective against PJ15 cells compared to PJ41. The combined therapy of HNSCC cells with anti-EGFR compounds shows that cetuximab did not affect cell proliferation, not even in combination, but TKIs and RAS inhibitor have pronounced antiproliferative effect on the two cell lines, which was much stronger on PJ15 cells than on PJ41 cells. Graphs show mean ± SD of four parallel samples, for single drug treatments, and two parallels of combination treatments, quantified as % of control (untreated cells). All values were measured in triplicates. (C) Flow cytometric determination of apoptotic nuclei (subG1 fraction). Erlotinib and zoledronic acid significantly increased the apoptosis in both HNSCC cell lines. However, c-MET-specific inhibitor SU11274 induced apoptosis in the PJ15 cells only. Cetuximab had no effect similarly to results of the proliferation assay. Data are means ± SD of three parallel samples “C”: cetuximab; “E”: erlotinib, “Z”: zoledronic acid; “SU”: SU11274.