| Literature DB >> 35152350 |
Tomofusa Fukuyama1,2, Toshio Kitamura3, Tomoko Kozu4.
Abstract
The chimeric oncogene AML1-MTG8 (RUNX1-RUNX1T1) is generated in t(8;21) acute myeloid leukemia (AML). Here, we report a novel interaction of MTG8/RUNX1T1/ETO with UBC9/UBE2I. AML1-MTG8 protein also interacted with UBC9, suggesting a role in leukemogenesis. Overexpression of UBC9 in Kasumi-1 attenuated myeloid differentiation induced by all-trans retinoic acid, G-CSF, and GM-CSF (AGGM), which was judged by suppression of CD11b. In addition, the UBC9 inhibitor 2-D08 accelerated myeloid differentiation induced by AGGM in two t(8;21) AML cell lines, Kasumi-1 and SKNO-1. These data suggest that UBC9 may play a role in leukemogenesis in t(8;21) AML by working with AML1-MTG8 to suppress myeloid differentiation. Therefore, UBC9 may be a good target for new differentiation therapy against t(8;21) AML.Entities:
Keywords: AML1; ETO; MTG8; RUNX1; UBC9
Mesh:
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Year: 2022 PMID: 35152350 DOI: 10.1007/s12185-022-03303-1
Source DB: PubMed Journal: Int J Hematol ISSN: 0925-5710 Impact factor: 2.490