BCR–ABL kinase activity rewires GM-CSFR signaling and confers oncogene addiction in TF1 cells. BCR–ABL kinase activity rewires GM-CSFR signaling and confers.

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BCR–ABL kinase activity rewires GM-CSFR signaling and confers oncogene addiction in TF1 cells. BCR–ABL kinase activity rewires GM-CSFR signaling and confers oncogene addiction in TF1 cells. A, percentage of cleaved caspase-3–negative population (live cells) of TF1/puro and TF1/BCR–ABL cells following 48 hours of treatment with, 0.2% dimethyl sulfoxide (DMSO), 2 ng/mL hGM-CSF, 100 nmol/L dasatinib, or 100 nmol/L dasatinib supplemented with 2 ng/mL of hGM-CSF. Active caspase-3 was measured by flow cytometry. Data represent average ± SD (n = 3; *, P < 0.001; two-way ANOVA with Bonferroni posttests). B, top, line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth factor stimulation. Bottom, Western immunoblot analysis of hGM-CSF–mediated (10′ stimulation) JAK2 activation, RAS–GTP loading, and activation of downstream effectors from whole-cell lysates in TF1/puro and TF1/BCR–ABL cells treated for 1 hour with 100 nmol/L dasatinib. The activation status of JAK2 was determined by immunoprecipitation and activation loop phosphorylation (Y1007). RAS activation was monitored using a RAS–GTP pull-down assay. C, top, line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth factor stimulation. Bottom, Western immunoblot analysis of hGM-CSF–mediated (10′ stimulation) RAS–GTP loading and activation of downstream effectors in TF1/puro and TF1/BCR–ABL cells after short-term and extended dasatinib treatment (100 nmol/L: 1, 2, 4, 8 hours). RAS activity was monitored as in B. D, normalized RAS–GTP loading in hGM-CSF–stimulated (10′) TF1/puro and TF1/BCR–ABL cells after prolonged dasatinib treatment (100 nmol/L, 24 hours). RAS activity was monitored as in B. RAS-GTP loading was normalized to the level observed in the “TF1/puro − DMSO + hGM-CSF” condition for each experimental replicate. Data represent the average ± SD (n = 3; **, P < 0.01; two-way ANOVA with Bonferroni posttests). E, top, line diagram representation of duration of serum starve, kinase inhibitor treatment, and growth factor stimulation. Bottom, Western immunoblot analysis of whole-cell lysates from TF1/puro and TF1/BCR–ABL cells after prolonged dasatinib treatment (100 nmol/L, 24 hours) and hGM-CSF stimulation (10′). IP, immunoprecipitation. Jennifer Asmussen et al. Cancer Discovery 2014;4:200-215 ©2014 by American Association for Cancer Research