EJ-A is a Balb-3T3 transfectant cell line that bears a small number of EJ-ras oncogene copies/cell, has low EJ-ras expression, and resembles the parental cell line in displaying a non-transformed phenotype. The glucocorticoid hormone dexamethasone reversibly induces transformation traits in EJ-A cells, namely: 1) morphological transformation; 2) increased growth rate and saturation density; 3) reduced GI length; and 4) independence of the FGF requirement to initiate DNA synthesis. Western blot analysis revealed that dexamethasone does not increase the p2 lm protein intracellular level. p-IFN, added to the culture medium, does not suppress the dexamethasone-induced growth stimulation and morphological transformation. Therefore, glucocorticoid hormones can complement low EJ-ras expression to transform Balb3T3 cells, by a mechanism that is likely to be independent of ~21'"" increase and P-IFN decrease.
Key words. EJ-ras oncogene tramfectant, glwmrticoid hormone, reversible tramformation, p 2 F , 8-IFN Reports from several laboratories described a variety of effects of glucocorticoid hormones upon cell-cycle regulation [l-71. More recently, it has been shown that glucocorticoids inhibit synthesis of peptide growth factors and interferon [8-121, hence, modulating cell growth and possibly expression of the transformed phenotype.
In this paper, we report that dexamethasone reversibly complements the transforming activity of mutated human c-Ha-ras-1 oncogene (EJ form) in Balb-3T3 mouse embryo cells. The mechanism underlying this dexamethasone effect does not seem to involve increased EJ-ras expression or inhibition of endogenous 0-IFN synthesis.
MATERIALS AND METHODS Cells
The original stock of early passage Balb-3T3, clone A3 1, came from Dr. Charles D. Stiles laboratory (Dana-Farber Cancer Institute, Boston). Cultures were maintained under strict regimen of cultivation: continuously growing from sparse to near confluent