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Blood, Vol. 110, Issue 6, 2084-2091, September 15, 2007
Low-dose arsenic trioxide sensitizes glucocorticoid-resistant acute lymphoblastic leukemia cells to dexamethasone via an Akt-dependent pathway
Blood Bornhauser et al.
110: 2084
Supplemental materials for Bornhauser et al, Vol. 110, Issue 6, 2084-2091
Files in this Data Supplement:
- Table S1. Number of PI positive cells as % of total cells (PDF, 13.9 KB)
- Figure S1. ATO does not sensitize CEM-C1 cells to commonly used chemotherapeutics (JPG, 29.1 KB)
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CEM-C1 cells were incubated with 0.5 µM ATO and indicated concentrations of cytotoxic drugs; cell viability was assessed using the MTT assay.
- Figure S2. MOLT-4 cells have functional p53, whereas CEM-C1, CEM-C7, and Jurkat cells have non-functional p53 as shown with the nutlin assay (JPG, 35.4 KB)
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Cell lines were incubated with indicated concentrations of nutlin, and cell viability was assessed with the MTT assay.
- Figure S3. ATO does not influence transactivation of the glucocorticoid receptor (JPG, 28.1 KB)
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CEM-C1 cells were transfected with the pMMTV-Luciferase reporter construct, which carries a GC-sensitive promoter in front of the luciferase reporter Lanz RB et al. Cell. 1999;97:17-27. Cells were cotransfected with a  -galactosidase construct for normalization. Transfected cells were treated as indicated, and transactivation activity of the GC receptor was assessed using luminometric analysis. In parallel, RNA was extracted from treated cells and reporter expression was analyzed by semi-quantitative RT-PCR using luciferase-specific primers.
- Figure S4. NF-κB is not activated upon ATO treatment (JPG, 25.5 KB)
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CEM-C1 cells were incubated with either PBS, 0.25 µM ATO, 1 µM Dex, or the combination; cytosolic and nuclear fractions were prepared and analyzed using the indicated antibodies.
- Figure S5. Rapamycin does not increase the GC-sensitizing effect of ATO (JPG, 38.9 KB)
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CEM-C1 cells were incubated with the indicated compounds; cell viability was assessed with the MTT assay.
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