Fig. 5From: Combining gene expression analysis of gastric cancer cell lines and tumor specimens to identify biomarkers for anti-HER therapies—the role of HAS2, SHB and HBEGFEffects of cetuximab and afatinib on proliferation after HBEGF knockdown or stimulation in MKN1 cells. MKN1 cells were transfected with negative-control (Ctr) or HBEGF (HBEGF KD) siRNA. Non-transfected (NT) cells were used as control. The knockdown was checked on RNA level on day 1 (d1) and day 5 (d5) after transfection a. The metabolic activity was measured by WST-1 proliferation assay for 72 h in the untreated b and treated c state. MKN1 cells were stimulated with 5 ng/ml HBEGF (+ HBEGF 5) or not stimulated (-HBEGF 5). The metabolic activity was measured by WST-1 proliferation assay for 72 h in the untreated d and treated e state. Cells were treated with 1 μg/ml cetuximab (Cet 1), 10 μg/ml cetuximab (Cet 10), 0.5 μM afatinib (Afa) or the corresponding solvents (Cet Solv, Afa Solv) for 72 h. Shown are the mean values from three experiments with standard deviation. Significant effects compared to untreated within a group (HBEGF KD, Ctr, NT (c) or + HBEGF 5, -HBEGF 5 (e)) are indicated by *p < 0.05, a** p < 0.01 or a***p < 0.001 (one-sample t-test). Significant effects compared to Ctr, NT (c) or –HBEGF (e) with the same treatment are indicated by b* p < 0.05 or b** p < 0.01 (two-sample t-test)Back to article page