GSE171976
STAT5 is insufficient to drive steroid resistance in T-cell acute lymphoblastic leukemia despite activation of BCL2 and BCLXL upon glucocorticoid treatment
Overexpression of STAT5B_N642H mutant results in the ligand-independent activation of STAT5 signaling and STAT5 transcriptional activity, without affecting MAPK-ERK or PI3K-AKT signalling pathways. Overexpression of wild type (WT) STAT5B did not activate STAT5 signaling . Treatment with prednisolone boosts the expression of STAT5_N642H regulated genes, whereas NR3C1 can bind at gene loci of STAT5 regulated genes. Despite the steroid-enhanced upregulation of anti-apoptotic targets, the mutant cell line remaind sensitive to steroid treatment. We studied potential co-regulation and co-binding of NR3C1 and STAT5B in STAT5B_N642H and STAT5B_WT overexpressing cells, treated and untreated with prednisolone. Overall design: NR3C1 and STAT5B binding for SUPT-1 cells overexpressing STAT5 wild type (WT) or STAT5 mutant (N642H), in the absence or presence of prednisolone treatment