Skip to main content
. 2016 Jun 8;44(4):855–864. doi: 10.1177/0300060516647550

Table 2.

Cell proliferation (CCK-8 assay), apoptosis, cell invasion and cell migration (wound healing rate) in the gastric adenocarcinoma cell line AGS following erlotinib treatment and/or transfection with small hairpin (sh)RNA targeting focal adhesion kinase (FAK).

Parameter Group
A B C D E
CCK-8 assay
24h 0.75 ± 0.03 0.74 ± 0.02 0.53 ± 0.06a 0.56 ± 0.04a 0.34 ± 0.04ab
48h 1.36 ± 0.01 1.41 ± 0.12 0.94 ± 0.12a 0.88 ± 0.08a 0.51 ± 0.03ab
72h 1.77 ± 0.17 1.83 ± 0.13 1.05 ± 0.10a 0.78 ± 0.08a 0.42 ± 0.03ab
96h 2.14 ± 0.20 2.10 ± 0.21 1.19 ± 0.12a 0.65 ± 0.03a 0.34 ± 0.05ab
Apoptosis Rate, % 7.3 ± 3.2 7.3 ± 2.0 35.0 ± 4.7a 45.2 ± 4.2a 59.1 ± 6.5ab
Cell invasion 65.8 ± 0.8 64.6 ± 0.9 51.2 ± 1.3a 21.7 ± 0.6a 13.7 ± 1.2ab
Wound healing rate, % 21.1 ± 0.9 21.3 ± 0.4 15.2 ± 0.8a 12.8 ± 0.6a 5.8 ± 0.6ab

Data presented as mean ± SD.

a

P < 0.05 vs Group A;

b

P < 0.05 vs Group C and D; one-way analysis of variance.

Group A, control group (nontransfected, no erlotinib); Group B, empty vector group (transfected with empty vector, no erlotinib); Group C, FAK group (transfected with FAK-shRNA, no erlotinib); Group D, erlotinib group (nontransfected, 40 µmol/l erlotinib); Group E, combination group (transfected with FAK-shRNA, 40 µmol/l erlotinib)