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

Figure 1

SOD3 mRNA expression level in the cell model systems used in this study. (a) SOD3 expression analysis in human papillary thyroid TPC1 and anaplastic thyroid 8505c cells showed significantly reduced mRNA expression compared to Nthy cells representing normal thyroid. (b) The sod3 mRNA expression from rat thyroid PC Cl3 cells modeling normal thyroid, PC PTC1 transformed with the PTC1 oncogene, and PC E1A cells transformed with the E1A oncogene. The oncogenic transformation of PC Cl3 cells caused a downregulation of sod3 mRNA. (c) The expression analysis of sod3 from rat FRLT5 cell clones harboring 1.4-fold to 46-fold increased RAS activity compared to control FRLT5 cells suggested significantly increased sod3 expression in the clones V13 (1.4-fold RAS activity), K20 (3.1-fold RAS activity), and K2 (6.3-fold RAS activity). A significant decrease in sod3 mRNA synthesis was observed in the clone V21 (10-fold RAS activity) that was further reduced in the clones V39 (35-fold RAS activity) and V27 (46-fold RAS activity). (d) The expression analysis of the microRNA mir21 from FRLT5 cells. Compared to control FRLT5 cells, the expression levels of mir21 were similar in the clones V13 (1.4-fold RAS activity), K20 (3.1-fold RAS activity), and K2 (6.3-fold RAS activity). A significant increase in expression was observed in the clones V21 (10-fold RAS activity), V39 (35-fold RAS activity), and V27 (46-fold RAS activity). The data are expressed as the mean ± SD. The values are represented (, , and ).

(a)

(b)

(c)

(d)