Title : Bortezomib sensitivity of acute myeloid leukemia CD34(+) cells can be enhanced by targeting the persisting activity of NF-κB and the accumulation of MCL-1.

Pub. Date : 2013 Jun

PMID : 23416210






5 Functional Relationships(s)
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1 Bortezomib sensitivity of acute myeloid leukemia CD34(+) cells can be enhanced by targeting the persisting activity of NF-kappaB and the accumulation of MCL-1. Bortezomib CD34 molecule Homo sapiens
2 In this study, we questioned whether leukemic stem cell-enriched CD34(+) cells are sensitive to the proteasome inhibitor bortezomib. Bortezomib CD34 molecule Homo sapiens
3 Surprisingly, we observed in short-term and long-term culture assays that CD34(-) AML cells were more sensitive to bortezomib treatment compared with the CD34(+) AML cells at a clinical relevant dosage. Bortezomib CD34 molecule Homo sapiens
4 The better survival of CD34(+) AML cells upon bortezomib treatment was due to a persisting NF-kappaB activity that could be overcome by the IKK inhibitor BMS-345541. Bortezomib CD34 molecule Homo sapiens
5 MCL-1 accumulated in CD34(+) AML cells upon bortezomib treatment and inhibition of MCL-1 by shRNA, or Obatoclax, significantly improved the sensitivity of CD34(+) AML cells to bortezomib. Bortezomib CD34 molecule Homo sapiens