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Fig. 5 | BMC Cancer

Fig. 5

From: 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 HBEGF

Fig. 5

Effects 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)

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