Figure 7
Figure 7. Prosurvival genes are differentially upregulated in CML cells vs normal cord blood cells. (A) CP CML and cord blood (CB) CD34+ progenitors (n = 3 each) were treated under normoxia or hypoxia for 96 hours and the RNA harvested for real-time polymerase chain reaction analysis by Fluidigm array. Results show the fold increase by hypoxia with respect to that of normoxia. The red line indicates the cutoff for genes with no hypoxic upregulation. Expression was normalized to that of TBP. Error bars represent standard of the mean. U.D., undetectable. (B) K562 cells were transduced with scrambled shRNA control or HIF1-α shRNA (n = 3). Cells were treated under normoxia or hypoxia for 48 hours, and the RNA were harvested for RT-PCR analysis by Fluidigm array. Results show the hypoxia-induced fold change in expression with respect to that of scrambled control treated with normoxia. Expression was normalized to TBP. Error bars represent standard of the mean. (C) Model showing the maintenance of CML progenitors under hypoxia and imatinib in the hypoxic BM environment.

Prosurvival genes are differentially upregulated in CML cells vs normal cord blood cells. (A) CP CML and cord blood (CB) CD34+ progenitors (n = 3 each) were treated under normoxia or hypoxia for 96 hours and the RNA harvested for real-time polymerase chain reaction analysis by Fluidigm array. Results show the fold increase by hypoxia with respect to that of normoxia. The red line indicates the cutoff for genes with no hypoxic upregulation. Expression was normalized to that of TBP. Error bars represent standard of the mean. U.D., undetectable. (B) K562 cells were transduced with scrambled shRNA control or HIF1-α shRNA (n = 3). Cells were treated under normoxia or hypoxia for 48 hours, and the RNA were harvested for RT-PCR analysis by Fluidigm array. Results show the hypoxia-induced fold change in expression with respect to that of scrambled control treated with normoxia. Expression was normalized to TBP. Error bars represent standard of the mean. (C) Model showing the maintenance of CML progenitors under hypoxia and imatinib in the hypoxic BM environment.

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