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. Author manuscript; available in PMC: 2009 Jul 1.
Published in final edited form as: Nat Med. 2008 Dec 21;15(1):50–58. doi: 10.1038/nm.1900

Figure 3.

Figure 3

BIM upregulation reverses glucocorticoid resistance in T-ALL cells treated with dexamethasone plus CompE. (a, b) Quantitative RT-PCR analysis of the BH3-only factors BIM (a) and BMF (b) in CUTLL1 cells treated with dexamethasone and/or CompE compared with vehicle only (DMSO). Relative expression levels are shown normalized to those of vehicle-only controls. (c) Western blot analysis and quantitation of BIM and BMF in CUTLL1 cells treated with dexamethasone and/or CompE compared with vehicle only (DMSO). (d) Western blot analysis of BIM following sRNA knock down. CUTLL1 cells infected with control lentivirus targeting the luciferase gene (pLKO LUC) or BIM (pLKO BIM) were treated with vehicle only or dexamethasone plus CompE for 24 hours and analyzed by Western blotting. (e) Induction of apoptosis in control (pLKO LUC infected) and BIM knockdown (pLKO BIM infected) cells treated with dexamethasone plus CompE. (f) Western blot analysis of BMF by shRNA knock down. CUTLL1 cells infected with control lentivirus targeting the luciferase gene (pLKO LUC) or BMF (pLKO BMF) were treated with vehicle only or dexamethasone plus CompE for 24 hours and analyzed by Western blot. (g) Induction of apoptosis in control (pLKO LUC infected) and BMF knockdown (pLKO BMF-infected) cells treated with dexamethasone plus CompE. Apoptosis refers to the percentage of annexin V positive/PI negative cells. (h) Schematic representation of the transcriptional regulatory network controlling glucocorticoid receptor autoregulation downstream of NOTCH1 and dexamethasone-induced apoptosis upon inhibition of NOTCH1 signaling via GSI treatment.

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