Abstract:
:CD56(high) acute myeloid leukemias (AMLs) have a poor prognosis, but it has been unclear how CD56 expression is controlled and how it relates to clinical aggressiveness. We show that CD56 expression on AML cells correlates with an abnormal expression pattern of runt-related transcription factor 1 (RUNX1) isoforms. Whereas full-length p48 RUNX1 (p48) up-regulated CD56 in AML cells, 3 previously unknown shorter RUNX1 isoforms, p38a, p30, and p24, suppressed CD56 expression. Both p48 and CD56 induced nuclear translocation of nuclear factor (NF)-kappaB and increased bcl2L12 expression, and inhibition of this pathway by small inhibitory RNA-mediated p48 knock down or NF-kappaB blockade substantially increased apoptosis in CD56(+) AML cell lines. These findings indicate the potential for new therapy of CD56(high) AML by suppression of the "overactive" RUNX1/CD56/NF-kappaB signaling pathway(s).
journal_name
Bloodjournal_title
Bloodauthors
Gattenloehner S,Chuvpilo S,Langebrake C,Reinhardt D,Müller-Hermelink HK,Serfling E,Vincent A,Marx Adoi
10.1182/blood-2007-02-074203subject
Has Abstractpub_date
2007-09-15 00:00:00pages
2027-33issue
6eissn
0006-4971issn
1528-0020pii
blood-2007-02-074203journal_volume
110pub_type
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