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Figure 2 | BMC Cancer

Figure 2

From: Increased p38-MAPK is responsible for chemotherapy resistance in human gastric cancer cells

Figure 2

Activation of p38 MAPK/AP-1 pathway in SGC7901/VCR cells. (A) SGC7901/VCR and SGC7901 cells were transfected with AP-1 luciferase reporter plasmids. After 24 hours, the cells were collected and luciferase assays were performed. The luciferase activity results in SGC7901 cells were normalized to 1.0. Error bars indicate standard deviations. The values shown represent the means of at least three separate experiments. Significant differences are indicated by asterisks. *, P < 0.05. (B) Levels of phosphorylated and non-phosphroylated MAP kinases (p38-MAPK, ERKs and JNKs) in SGC7901/VCR and SGC7901 cells were detected using Western-blot analyses. A representative example of an experiment that was repeated three times is shown. (C) FACS analysis of p38-MAPK, ERK and JNK phosphorylation. A representative example of an experiment that was repeated three times is shown. (D-E) Analysis of AP-1 activity using the luciferase assay in SGC7901/VCR cells treated or untreated with SB202190 (10 μM), or cotransfected with the DN-p38 plasmid for 24 hours. The luciferase activity in control samples was normalized to 1.0. Error bars indicate standard deviations. The values shown represent the means of at least three separate experiments. Significant differences are indicated by asterisks. *, P < 0.05. (F) SGC7901 cells were incubated with cisplatin (2 μg/ml) for 24 h, and then cells were collected. FACS analysis was used to detect p38-MAPK phosphorylation.

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