Mutated N-ras does not induce p19arf in CO25 cell line

Abstract

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 p19^arf and MDM2 genes under the effect of N-ras oncogene induction and to invent the role of p19^arf, 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 p19^arf 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 p19^arf 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 p19^arf lack system.

Key words: Oncogene, N-ras, p19^arf, myoblast, CO25 cells, differentiation, MDM2.