Mutated N-ras does not induce p19arf in CO25 cell line
The mouse cell line (CO25) used in this study was transfected with a glucocorticoid inducible mutated human N-ras oncogene under transcriptional control of the steroid-sensitive promoter of the mouse mammary tumors virus long terminal repeat MMTV-LTR. This study was aimed to investigate the expression of p19arf and MDM2 genes under the effect of N-ras oncogene induction and to invent the role of p19arf, MDM2 in N-ras pathway during various periods (12, 24, 48, 72, 96 h) using western blotting method. The levels of â-actin proteins in the same periods were our control group. The observations showed no increase of p19arf protein expression in normal, cancer and differentiated CO25 cells. MDM2 was accumulated until 72 h and after 96 h, it showed a dramatical decrease while β-actin levels were increased correlated to the volume of protein loaded to the gel. Because of the role of p19arf as tumor suppressor and p53-MDM2 linker, it is highly recommended to investigate the relationship between N-ras and p53 and MDM2 in the same system to recognize the molecule that may play a linker molecule between p53 and MDM2 in p19arf lack system.
Key words: Oncogene, N-ras, p19arf, myoblast, CO25 cells, differentiation, MDM2.