Ras Oncogene-Mediated Progressive Silencing of Extracellular Superoxide Dismutase in Tumorigenesis

Figure 2

Effect of the p38 MAPK inhibitor SB202190 on SOD3 mRNA expression. (a–c) The inhibition of p38 MAPK phosphorylation increased the SOD3 expression in human TPC1 and 8505c cells, while SB202190 treatment did not alter the SOD3 mRNA synthesis in Nthy cells modeling normal thyroid. (d–f) The inhibitor treatment increased sod3 mRNA expression in PC Cl3-derived PC PTC1 and PC E1A cells, while the treatment had no effect on PC Cl3 control cells modeling normal thyroid. (g–j) FRLT5 cell clones V13, V21, and V39 stably transfected with RAS showed a significant increase in sod3 mRNA expression after SB202190 treatment, whereas SB202190 had no effect on FRLT5 control cells, which is consistent with the results using the other cell models. (k, m) The Western blot analysis for p38 MAPK activation in FRLT5 control cells, clone V13, clone V21, and clone V39. The histogram (panel (m)) suggested significantly increased p38 MAPK phosphorylation in FRLT5-derived clones compared to control cells. Total p38 MAPK was used to normalize the phosphorylation level. (l, n) The transient transfection of an H-RasV12 expression plasmid into HEK 293T cells showed a gradual increase in p38 MAPK phosphorylation that corresponded to the amount of plasmid transfected. Total p38 MAPK was used to normalize the phosphorylation level. The data are expressed as the mean ± SD. The values are represented (, , and ).

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