Figure 2
Cell growth inhibition. (a) N87 cells treated with Tmab, 5-FU, and CDDP. (b) OE19 cells treated with Tmab, 5-FU, and CDDP. (c) NCI-N87 cells treated with PI3K inhibitors. (d) OE19 cells treated with PI3K inhibitors. (e) NCI-N87 cells treated with PI3K inhibitors and Tmab. (f) OE19 cells treated with PI3K inhibitors and Tmab. Cell viability was measured using the WST-8 colorimetric assay. PTEN knockdown was performed with shRNA (shPTEN#1 and shPTEN#2). Treatment was performed for 120 h using the following conditions: Tmab (10 μg/mL), 5-FU (1 µM for NCl-N87 cells and 10 µM for OE19 cells), CDDP (1 µM), LY294002 (5 µM for NCl-N87 cells and 10 µM for OE19 cells), everolimus (10 nM), MK-2206 (500 nM for NCl-N87 cells and 5 µM for OE19 cells), and NVP-BEZ235 (50 nM for NCl-N87 cells and 500 nM for OE19 cells). Cell growth inhibition was calculated using the following formula: [1 − experimental absorbance (treated well)/control absorbance (untreated well)] × 100; except for (a) and (b), all values are expressed as a ratio with the value of the scrambled cells set as 100%. n = 3 in each group. (g) Influence of PI3K inhibitors on NCl-N87 cells. Western blotting analysis of PI3K and MAPK. PTEN knockdown was achieved using siRNA (siPTEN#1 and siPTEN#2). The treatment duration was 24 h, and the concentrations were the same as above. *p < 0.05, **p < 0.001 using Student’s t test. #1a was siPTEN#1, #2a was siPTEN#2.
