Fig. 4

NR3C1 disrupts the mitochondrial apoptosis axis in ALL cells. a Transcriptome sequencing of ex vivo-cultured wild-type Reh cells (GC-resistant) and Reh cells with ectopic expression of NR3C1 (GC-sensitive) following exposure to dexamethasone. Pathway analysis of genes regulated by NR3C1 in the indicated ALL cell line. b Significantly increased expression of pro-apoptotic genes and decreased transcription of anti-apoptotic genes were observed in Reh cells with ectopic expression of NR3C1. c Western blotting analysis of expression of the pro-apoptotic proteins and anti-apoptotic proteins in GC-resistant Reh and Jurkat ALL cells ectopically expressing NR3C1. d Western blotting analysis of expression of the pro-apoptotic proteins and anti-apoptotic proteins in GC-sensitive CCRF-CEM, 6T-CEM and NALM6 cells with NR3C1 gene knockdown. e Comparison of mRNA expression of the pro-apoptotic genes and anti-apoptotic genes in bone marrow blast samples from patients of good responders to prednisolone (n = 10) and patients with refractory or relapsed ALL (n = 20). In the bottom, western blotting analysis of the concentration of NR3C1 protein in ALL cells from 3 patients in the good-responder cohort and from 3 R/R ALL patients