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Background and aims: Glucocorticoids (GCs) have been successfully employed in the treatment of human leukemia; however, those effects can be deteriorated as the metabolic side effects occurred due to the activation glucocorticoid-induced leucine zipper (GILZ) leading to the induction of the GC resistance which is initiated via the Ets-related gene (Erg). In the present work, we recruited this antagonist influence on ERG for aiming to understand the physiological potential that might be of benefit in the treatment of leukemia using a non-steroidal compound (CPDA). Methods: We examined the effect of dexamethasone, as a steroid, and CPDA, as a non-steroid substance, on the GILZ and ERG receptor gene expression in The chicken leukemia cells (CLCs), DT40 cells, after treating them with the drug at 1μM followed by a 24-hour incubation. A real-time-polymerase chain reaction (RT-PCR) method was used to measure gene expression. Results: An increase (two-fold) in the expression of GILZ receptor was unveiled. This enhanced-GILZ model presents the steroidal positive actions and refers to the CPDA ability to mimic this action of steroids. The results also demonstrated a downregulation in the mRNA expression level of ERG, indicating of antagonism of steroids in responding cells and as a positive finding for the effect of the non-steroidal compound A tested. Conclusions: Steroid-induced upregulation in the GILZ receptor provides proof of GC undesirable effects leading to correlated ERG-initiated resistance to the steroids used in exposed cells. Interestingly, CPDA has a GC-based treating activity low GILZ expression.

Modulation of GILZ and Erg upon Non-Steroidal Treatment in Chicken Leukemic Cells